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bibo:doi: 10.3390%2Fmolecules16064567
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Subject Item: _:vb11323152
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dc:title: conclusions
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Subject Item: _:vb11323153
rdf:type: n3:Context
rdf:value: Genome instability and immune guided inflammatory reactions lead to the development of tumour microenvironment [>>164<<]. In the last three decades, the introduction of mechanism-based targeted therapies to treat human cancers provided better understanding of the mechanism in cancer pathogenesis. Some examples of selected therapeutic targeting are listed
n3:mentions: n2:21376230

Subject Item: _:vb11323154
rdf:type: n3:Context
rdf:value: This table is modified from the illustration given by Hanahan and Weinberg [>>164<<].
n3:mentions: n2:21376230

Subject Item: _:vb11323155
rdf:type: n3:Context
rdf:value: This concept is exemplified by recent discoveries [>>165<<,166,167]. Therefore, a multi-targeted molecule, such as curcumin, might be better choice for the treatment of cancer.
n3:mentions: n2:20236818

Subject Item: _:vb11323156
rdf:type: n3:Context
rdf:value: This concept is exemplified by recent discoveries [165,>>166<<,167]. Therefore, a multi-targeted molecule, such as curcumin, might be better choice for the treatment of cancer.
n3:mentions: n2:19671869

Subject Item: _:vb11323157
rdf:type: n3:Context
rdf:value: This concept is exemplified by recent discoveries [165,166,>>167<<]. Therefore, a multi-targeted molecule, such as curcumin, might be better choice for the treatment of cancer.
n3:mentions: n2:18650835

Subject Item: _:vb11323158
rdf:type: n3:Context
rdf:value: years, a number of studies have provided evidence for several pharmacological properties of curcumin including chemosensitizing, radiosensitizing, wound healing, antimicrobial, antiviral, antifungal, and anti-inflammatory activities [>>168<<]. Curcumin has been shown to inhibit several cell signalling pathways at multiple levels, affecting the expression and activity of cellular enzymes such as COX and GSTs, and influencing immunomodulation, angiogenesis, and cell-cell
n3:mentions: n2:18655004

Subject Item: _:vb11323159
rdf:type: n3:Context
rdf:value: Use of a standardized extract such as Polyphenone E, a topical antiviral cream based on purified green tea extract has been approved as a prescription drug by FDA in 2006, would be the new trend in pharmaceutical sciences [>>169<<]. Similarly, potentially beneficial interactions between diet-derived polyphenols and other drugs and between individual components of the human diet have been identified. Examples of this concept include the combination of curcumin with
n3:mentions: n2:17576417

Subject Item: _:vb11323160
rdf:type: n3:Context
rdf:value: Examples of this concept include the combination of curcumin with the green tea extract, epigallocatechin-3-gallate (EGCG) [>>170<<]; curcumin combined with the flavonoid quercetin, found in apples, onions, and citrus fruits [118].
n3:mentions: n2:9525275

Subject Item: _:vb11323161
rdf:type: n3:Context
rdf:value: Examples of this concept include the combination of curcumin with the green tea extract, epigallocatechin-3-gallate (EGCG) [170]; curcumin combined with the flavonoid quercetin, found in apples, onions, and citrus fruits [>>118<<]. Interactions relevant to combinatorial treatment with curcumin might be important due to alteration in absorption, cellular and biological responses. For example, the combination of curcumin and genistein (a natural product derived from
n3:mentions: n2:16757216

Subject Item: _:vb11323162
rdf:type: n3:Context
rdf:value: For example, the combination of curcumin and genistein (a natural product derived from soya beans) appears to strongly inhibit growth of human breast MCF-7 cells synergistically [>>171<<]. It is also evident that the toxic effect of drugs like 5-flurouracil vinorelbine can be reduced by combined treatment with curcumin [172,173].
n3:mentions: n2:9168916

Subject Item: _:vb11323163
rdf:type: n3:Context
rdf:value: It is also evident that the toxic effect of drugs like 5-flurouracil vinorelbine can be reduced by combined treatment with curcumin [>>172<<,173].
n3:mentions: n2:16340194

Subject Item: _:vb11323164
rdf:type: n3:Context
rdf:value: It is also evident that the toxic effect of drugs like 5-flurouracil vinorelbine can be reduced by combined treatment with curcumin [172,>>173<<].
n3:mentions: n2:15883009

Subject Item: _:vb11323165
rdf:type: n6:Section
dc:title: background
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Subject Item: _:vb11323166
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rdf:value: In addition, many of them play important roles in regulating the immune system and are now being investigated as chemopreventive, neuroprotective, cardioprotective and hepatoprotective agents, either acting alone or in combinations [>>1<<,2]. In particular, turmeric, a typical example of polyphenol-rich natural remedies, has been used for centuries in Indian traditional medicine (Ayurveda) and Traditional Chinese Medicine (TCM) [2].
n3:mentions: n2:14612489

Subject Item: _:vb11323167
rdf:type: n3:Context
rdf:value: characterized as safe by the Food and Drug Administration (FDA) in the USA, the Natural Health Products Directorate of Canada, and the Joint Expert Committee of the Food and Agriculture Organization/World Health Organization (FAO/WHO) [>>3<<]. Curcumin, a principal polyphenol component of turmeric, is available as an over-the-counter (OTC) supplement worldwide.
n3:mentions: n2:9154169

Subject Item: _:vb11323168
rdf:type: n3:Context
rdf:value: the inflammation associated with experimental colitis, including a substantial reduction of the rise in myleoperoxidase (MPO) activity, an established marker for inflammatory cells (mainly polymorphonuclear leukocytes) and TNF-α [>>6<<,7]. In addition, curcumin is able to reduce colonic nitrite levels and downregulate cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) expression and p38 mitogen activated protein kinase (MAPK) activation [6,7].
n3:mentions: n2:20955148

Subject Item: _:vb11323169
rdf:type: n3:Context
rdf:value: In addition, curcumin is able to reduce colonic nitrite levels and downregulate cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) expression and p38 mitogen activated protein kinase (MAPK) activation [>>6<<,7]. In spite of the abundant evidence at the molecular level, and extensive studies at the preclinical and clinical levels, its therapeutic outcome remains a challenge owing to its low solubility and poor bioavailability. Therefore, this
n3:mentions: n2:20955148

Subject Item: _:vb11323170
rdf:type: n6:Section
dc:title: turmeric history
n6:contains: _:vb11323171

Subject Item: _:vb11323171
rdf:type: n3:Context
rdf:value: was published in 1748, and the first pharmacologic review of turmeric appeared 67 years later [>>3<<,13].
n3:mentions: n2:9154169

Subject Item: _:vb11323172
rdf:type: n6:Section
dc:title: curcumin chemistry
n6:contains: _:vb11323173 _:vb11323174 _:vb11323175 _:vb11323176

Subject Item: _:vb11323173
rdf:type: n3:Context
rdf:value: Its chemical structure was confirmed in 1973 by Roughley and Whiting [15] and the solution structure was only confirmed in 2007 by Payton et al. [>>16<<].
n3:mentions: n2:17315954

Subject Item: _:vb11323174
rdf:type: n3:Context
rdf:value: In solution, it has been demonstrated that 90% of curcumin was found degraded to trans-6-(4’-hydroxy-3’-methoxyphenyl)-2,4-dioxo-5-hexanal, vanillin, feruloylmethane, and ferulic acid within 30 minutes [>>19<<]. Curcumin is similarly unstable at basic pH, but in presence of calf serum or human blood less than 20% of curcumin was found to be decomposed in 1 h [20]. Addition of antioxidants (ascorbic acid, N-acetylcysteine or glutathione) to
n3:mentions: n2:11237176

Subject Item: _:vb11323175
rdf:type: n3:Context
rdf:value: Curcumin is similarly unstable at basic pH, but in presence of calf serum or human blood less than 20% of curcumin was found to be decomposed in 1 h [>>20<<]. Addition of antioxidants (ascorbic acid, N-acetylcysteine or glutathione) to culture media also inhibited the degradation of curcumin. Yellow curcumin changes to dark red colour at alkaline pH and under physiological conditions the λmax
n3:mentions: n2:9278892

Subject Item: _:vb11323176
rdf:type: n3:Context
rdf:value: Yellow curcumin changes to dark red colour at alkaline pH and under physiological conditions the λmax for curcumin is observed at 420 nm [>>21<<].
n3:mentions: n2:3765852

Subject Item: _:vb11323177
rdf:type: n6:Section
dc:title: curcumin safety and toxicity
n6:contains: _:vb11323178 _:vb11323179 _:vb11323180 _:vb11323181 _:vb11323182 _:vb11323183 _:vb11323184 _:vb11323185 _:vb11323186 _:vb11323187 _:vb11323188 _:vb11323189 _:vb11323190 _:vb11323191 _:vb11323192 _:vb11323193

Subject Item: _:vb11323178
rdf:type: n3:Context
rdf:value: 50 mg/day of curcumin [>>22<<]. In India, where the average intake of turmeric can be as high as 2,000–2,500 mg per day (corresponding to approx.
n3:mentions: n2:10616954

Subject Item: _:vb11323179
rdf:type: n3:Context
rdf:value: up to 100 mg of curcumin), no toxicities or adverse effects have been reported or studied at the population level [>>23<<]. However the doses administered in clinical trials are expected to be rather higher than those normally consumed in the diet. This fact underlines the need for systematic safety and toxicity studies. Based on repeated studies, turmeric
n3:mentions: n2:12676044

Subject Item: _:vb11323180
rdf:type: n3:Context
rdf:value: Based on repeated studies, turmeric is Generally Recognized As Safe (GRAS) by the US FDA, and curcumin has been granted an acceptable daily intake level of 0.1–3 mg/kg-BW by the Joint FAO/WHO Expert Committee on Food Additives, 1996 [>>3<<].
n3:mentions: n2:9154169

Subject Item: _:vb11323181
rdf:type: n3:Context
rdf:value: systematic studies funded by the Prevention Division of the US National Cancer Institute (NCI) conducted in rats, dogs, or monkeys and at oral doses of curcumin up to 3,500 mg/kg-BW for up to 90 days, no adverse effects were observed [>>3<<]. In a preclinical study involving the administration of 2% dietary curcumin (approx.
n3:mentions: n2:9154169

Subject Item: _:vb11323182
rdf:type: n3:Context
rdf:value: 1,200 mg/kg-BW) to rats for 14 days [>>24<<] or in a study of 0.2% dietary curcumin (approx.
n3:mentions: n2:11350917

Subject Item: _:vb11323183
rdf:type: n3:Context
rdf:value: Furthermore, a reproductive toxicity study with the oral curcumin administration of up to 1,000 mg/kg-BW daily, no toxicity was observed in two successive generations in rats [>>26<<].
n3:mentions: n2:16987575

Subject Item: _:vb11323184
rdf:type: n3:Context
rdf:value: In a study performed in India, daily administration of 1,200–2,100 mg of oral curcumin to patients with rheumatoid arthritis for 2–6 weeks did not cause any toxicity [>>27<<]. In another study of high-dose oral curcumin by Cheng et al. in Taiwan, administration of 500, 1,000, 2,000, 4,000, and 8,000 mg of curcumin daily for three months to patients with preinvasive malignant or high risk premalignant
n3:mentions: n2:7390600

Subject Item: _:vb11323185
rdf:type: n3:Context
rdf:value: et al. in Taiwan, administration of 500, 1,000, 2,000, 4,000, and 8,000 mg of curcumin daily for three months to patients with preinvasive malignant or high risk premalignant conditions, no noticeable adverse effects were detected [>>28<<]. Lao et al. studied safety of curcumin in healthy volunteers using curcumin capsules (containing 75% curcumin, 23% demethoxycurcumin and 2% bisdemethoxycurcumin) with single escalating doses from 500 mg to 12,000 mg.
n3:mentions: n2:11712783

Subject Item: _:vb11323186
rdf:type: n3:Context
rdf:value: In this study, the maximum tolerated dose could not be determined because more than 12,000 mg of curcumin is regarded as too bulky [>>29<<].
n3:mentions: n2:16545122

Subject Item: _:vb11323187
rdf:type: n3:Context
rdf:value: clinical trial on oral curcumin in patients with advanced colorectal cancer in which the US NCI criteria were used to assess potential toxicity, curcumin was well tolerated at all dose levels up to 3,600 mg daily for up to four months [>>30<<]. Adverse effects related to curcumin consumption reported by patients in these studies were mainly gastrointestinal (nausea and diarrhoea).
n3:mentions: n2:15501961

Subject Item: _:vb11323188
rdf:type: n3:Context
rdf:value: in traditional Asian medical systems, it should be noted by potential laboratory and clinical investigators that a few reports of allergic dermatitis after contact with curcumin have been published in the scientific literature [>>31<<,32,33]. An allergic reaction to turmeric-related products was also described in one healthy volunteer enrolled in a phase I study testing the safety of turmeric oil and turmeric extract [34].
n3:mentions: n2:2960490

Subject Item: _:vb11323189
rdf:type: n3:Context
rdf:value: in traditional Asian medical systems, it should be noted by potential laboratory and clinical investigators that a few reports of allergic dermatitis after contact with curcumin have been published in the scientific literature [31,>>32<<,33]. An allergic reaction to turmeric-related products was also described in one healthy volunteer enrolled in a phase I study testing the safety of turmeric oil and turmeric extract [34].
n3:mentions: n2:17150169

Subject Item: _:vb11323190
rdf:type: n3:Context
rdf:value: in traditional Asian medical systems, it should be noted by potential laboratory and clinical investigators that a few reports of allergic dermatitis after contact with curcumin have been published in the scientific literature [31,32,>>33<<]. An allergic reaction to turmeric-related products was also described in one healthy volunteer enrolled in a phase I study testing the safety of turmeric oil and turmeric extract [34].
n3:mentions: n2:16958931

Subject Item: _:vb11323191
rdf:type: n3:Context
rdf:value: been speculated that Curcuma extract (rather than curcumin) may potentially interfere with histamine 2-receptors antagonists (e.g., ranitidine) and proton-pump inhibitors (e.g., omeprazole) via inhibitory effects on histamine receptors [>>35<<]. Based on animal studies, other scientists have proposed that curcumin may enhance the hypoglycaemic effect of anti-diabetic medication or the efficacy of anti-lipemic drugs, via inhibition of the CYP enzyme system or reducing the
n3:mentions: n2:16327153

Subject Item: _:vb11323192
rdf:type: n3:Context
rdf:value: have proposed that curcumin may enhance the hypoglycaemic effect of anti-diabetic medication or the efficacy of anti-lipemic drugs, via inhibition of the CYP enzyme system or reducing the low-density lipoprotein fraction in the blood [>>36<<,37].
n3:mentions: n2:9046034

Subject Item: _:vb11323193
rdf:type: n3:Context
rdf:value: proposed that curcumin may enhance the hypoglycaemic effect of anti-diabetic medication or the efficacy of anti-lipemic drugs, via inhibition of the CYP enzyme system or reducing the low-density lipoprotein fraction in the blood [36,>>37<<].
n3:mentions: n2:16406419

Subject Item: _:vb11323194
rdf:type: n6:Section
dc:title: curcumin bioavailability
n6:contains: _:vb11323196 _:vb11323197 _:vb11323198 _:vb11323199 _:vb11323195 _:vb11323208 _:vb11323209 _:vb11323204 _:vb11323205 _:vb11323206 _:vb11323207 _:vb11323200 _:vb11323201 _:vb11323202 _:vb11323203

Subject Item: _:vb11323195
rdf:type: n3:Context
rdf:value: In another study, absorption of oral curcumin reported on 60% and glucuronide and sulphate conjugates detected in the urine [>>39<<]. Ravindranath et al. reported that the majority of the oral dose was found to be excreted in faeces, while approx. 35% was excreted unchanged, and the remaining 65% excreted as metabolites of curcumin [40]. After intravenous and
n3:mentions: n2:7423534

Subject Item: _:vb11323196
rdf:type: n3:Context
rdf:value: 35% was excreted unchanged, and the remaining 65% excreted as metabolites of curcumin [>>40<<]. After intravenous and intraperitoneal administration of curcumin in rats, large quantities of this compound and its metabolites were excreted in the bile, mainly as tetrahydrocurcumin and hexahydrocurcumin glucuronides (Figure 3)
n3:mentions: n2:7256789

Subject Item: _:vb11323197
rdf:type: n3:Context
rdf:value: After intravenous and intraperitoneal administration of curcumin in rats, large quantities of this compound and its metabolites were excreted in the bile, mainly as tetrahydrocurcumin and hexahydrocurcumin glucuronides (Figure 3) [>>41<<,42]. These data offered evidence in favour of the hypotheses that curcumin undergoes transformation during absorption via the intestine and that it is possibly subject to enterohepatic recirculation [40]. These data are in accordance with
n3:mentions: n2:7342372

Subject Item: _:vb11323198
rdf:type: n3:Context
rdf:value: After intravenous and intraperitoneal administration of curcumin in rats, large quantities of this compound and its metabolites were excreted in the bile, mainly as tetrahydrocurcumin and hexahydrocurcumin glucuronides (Figure 3) [41,>>42<<]. These data offered evidence in favour of the hypotheses that curcumin undergoes transformation during absorption via the intestine and that it is possibly subject to enterohepatic recirculation [40].
n3:mentions: n2:726520

Subject Item: _:vb11323199
rdf:type: n3:Context
rdf:value: These data offered evidence in favour of the hypotheses that curcumin undergoes transformation during absorption via the intestine and that it is possibly subject to enterohepatic recirculation [>>40<<]. These data are in accordance with the original hypothesis proposed by the researchers who studied the fate of curcumin in rats in 1978 [42].
n3:mentions: n2:7256789

Subject Item: _:vb11323200
rdf:type: n3:Context
rdf:value: These data are in accordance with the original hypothesis proposed by the researchers who studied the fate of curcumin in rats in 1978 [>>42<<].
n3:mentions: n2:726520

Subject Item: _:vb11323201
rdf:type: n3:Context
rdf:value: administration of curcumin (100 mg/kg) in mice, and have suggested that curcumin is first biotransformed to dihydrocurcumin and tetrahydrocurcumin, and that these compounds are subsequently converted to monoglucuronide conjugates [>>43<<]. Ireson et al. showed that small quantities of curcumin, hexahydrocurcumin, hexahydrocurcuminol, and hexahydro-curcumin glucuronide were present in plasma with higher levels of curcumin glucuronide and curcumin sulphate after oral dosing
n3:mentions: n2:10101144

Subject Item: _:vb11323202
rdf:type: n3:Context
rdf:value: that small quantities of curcumin, hexahydrocurcumin, hexahydrocurcuminol, and hexahydro-curcumin glucuronide were present in plasma with higher levels of curcumin glucuronide and curcumin sulphate after oral dosing of curcumin in rats [>>44<<]. Interestingly, the transformation of curcumin to its metabolites occurred more extensively in rat hepatocytes grown ex vivo than in human hepatocytes.
n3:mentions: n2:11221833

Subject Item: _:vb11323203
rdf:type: n3:Context
rdf:value: 1,200 mg/kg-BW) in F344 rats for 14 days showed that low nanomolar levels of parent compound are detectable in plasma, with concentrations in liver and colon mucosal tissue ranging from 0.1 to 1.8 nmol/g tissue [>>24<<].
n3:mentions: n2:11350917

Subject Item: _:vb11323204
rdf:type: n3:Context
rdf:value: In a study using high doses of oral curcumin (2,000 mg/kg) in rats, the investigators found that co-administration of piperine increased systemic bioavailability by as much as 154% [>>46<<]. The mechanism of this effect has not been elucidated yet.
n3:mentions: n2:9619120

Subject Item: _:vb11323205
rdf:type: n3:Context
rdf:value: In one of the studies, 2,000 mg of pure curcumin powder was administered to fasting volunteers and low curcumin concentrations in plasma (<10 ng/mL) were observed 1 h after the dose [>>46<<]. In the same study, concomitant administration of 20 mg of piperine appeared to increase bioavailability of curcumin in humans by 2,000%. In a study with higher doses of oral curcumin, Cheng et al. in Taiwan administered up to 8,000 mg
n3:mentions: n2:9619120

Subject Item: _:vb11323206
rdf:type: n3:Context
rdf:value: It was found that peak serum curcumin concentrations were achieved 1–2 h after oral intake as 1.75 μM and that levels gradually declined within 12 h [>>28<<]. In a dose-escalation study performed in the US, too low serum concentration of curcumin was observed (in some cases could not be detected) on administering 50–200 mg of oral micronized curcumin together with orange juice in healthy
n3:mentions: n2:11712783

Subject Item: _:vb11323207
rdf:type: n3:Context
rdf:value: No evidence of clinical toxicity attributable to the extract was detected, however, no evidence of detectable systemic bioavailability was observed either [>>48<<]. In a subsequent phase I study in 15 patients, a curcuminoid formulation was administered orally for up to four months, allowing rapid dose escalation and equating to curcumin doses between 450 and 3,600 mg daily [46]. Oral consumption
n3:mentions: n2:11448902

Subject Item: _:vb11323208
rdf:type: n3:Context
rdf:value: In a subsequent phase I study in 15 patients, a curcuminoid formulation was administered orally for up to four months, allowing rapid dose escalation and equating to curcumin doses between 450 and 3,600 mg daily [>>46<<]. Oral consumption of the highest dose of curcumin (3,600 mg daily) resulted in detectable levels of drug and conjugates in plasma, just above the limit of detection of the assay (approx. 0.63 ng/mL). Surprisingly, analysis of urine from
n3:mentions: n2:9619120

Subject Item: _:vb11323209
rdf:type: n3:Context
rdf:value: To determine levels of curcumin in gastrointestinal tissues, further studies were performed in patients undergoing operations for colorectal cancer who offered voluntary consent to have their tissues used for research purposes [49,>>50<<]. Twelve patients with histologically confirmed colorectal cancer received oral curcumin (450, 1,800, or 3,600 mg daily) for seven days before surgery.
n3:mentions: n2:14997198

Subject Item: _:vb11323210
rdf:type: n6:Section
dc:title: curcumin in inflammation and cancer
n6:contains: _:vb11323276 _:vb11323277 _:vb11323278 _:vb11323279 _:vb11323272 _:vb11323273 _:vb11323274 _:vb11323275 _:vb11323268 _:vb11323269 _:vb11323270 _:vb11323271 _:vb11323264 _:vb11323265 _:vb11323266 _:vb11323267 _:vb11323292 _:vb11323293 _:vb11323288 _:vb11323289 _:vb11323290 _:vb11323291 _:vb11323284 _:vb11323285 _:vb11323286 _:vb11323287 _:vb11323280 _:vb11323281 _:vb11323282 _:vb11323283 _:vb11323212 _:vb11323213 _:vb11323214 _:vb11323215 _:vb11323211 _:vb11323228 _:vb11323229 _:vb11323230 _:vb11323231 _:vb11323224 _:vb11323225 _:vb11323226 _:vb11323227 _:vb11323220 _:vb11323221 _:vb11323222 _:vb11323223 _:vb11323216 _:vb11323217 _:vb11323218 _:vb11323219 _:vb11323244 _:vb11323245 _:vb11323246 _:vb11323247 _:vb11323240 _:vb11323241 _:vb11323242 _:vb11323243 _:vb11323236 _:vb11323237 _:vb11323238 _:vb11323239 _:vb11323232 _:vb11323233 _:vb11323234 _:vb11323235 _:vb11323260 _:vb11323261 _:vb11323262 _:vb11323263 _:vb11323256 _:vb11323257 _:vb11323258 _:vb11323259 _:vb11323252 _:vb11323253 _:vb11323254 _:vb11323255 _:vb11323248 _:vb11323249 _:vb11323250 _:vb11323251

Subject Item: _:vb11323211
rdf:type: n3:Context
rdf:value: The functional relation between inflammation and cancer was hypothesized by Virchow already in 1863 [>>51<<]. Recent data have expanded the concept that inflammation is a critical component of tumor progression.
n3:mentions: n2:11229684

Subject Item: _:vb11323212
rdf:type: n3:Context
rdf:value: level inflammation that can persist over 20 to 30 years; eventually leading to cancer as well as other chronic diseases. Pro-inflammatory factors might be external such as environmental pollutants, viruses, bacteria, food, stress, etc. [>>52<<]. Several immune cells and their products guide and connect the inflammation reaction to the cancer progression.
n3:mentions: n2:12490959

Subject Item: _:vb11323213
rdf:type: n3:Context
rdf:value: The principal target molecules of internal pro-inflammatory factors responsible for mediating the inflammation are the free radicals, IL-1β, TNF-α, NF-κB, and NSAID-activated gene-1 (NAG-1) [53,>>54<<,55]. Although these molecules are essential for normal cell regulation processes, uncontrolled and too high exposure to such molecules can lead to chronic diseases (Figure 4) [52].
n3:mentions: n2:16563357

Subject Item: _:vb11323214
rdf:type: n3:Context
rdf:value: The principal target molecules of internal pro-inflammatory factors responsible for mediating the inflammation are the free radicals, IL-1β, TNF-α, NF-κB, and NSAID-activated gene-1 (NAG-1) [53,54,>>55<<]. Although these molecules are essential for normal cell regulation processes, uncontrolled and too high exposure to such molecules can lead to chronic diseases (Figure 4) [52].
n3:mentions: n2:18089954

Subject Item: _:vb11323215
rdf:type: n3:Context
rdf:value: Although these molecules are essential for normal cell regulation processes, uncontrolled and too high exposure to such molecules can lead to chronic diseases (Figure 4) [>>52<<].
n3:mentions: n2:12490959

Subject Item: _:vb11323216
rdf:type: n3:Context
rdf:value: enzymes such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), together with the nonenzymatic system such as glutathione and vitamins (A, C, and E) defense against over-reaction of free radicals [>>56<<]. In addition to this, other molecules like polyphenols, ubiquinol-10, glucose and albumin, as well as minerals, such as selenium and zinc, can also counteract free radical activity.
n3:mentions: n2:11089981

Subject Item: _:vb11323217
rdf:type: n3:Context
rdf:value: balance of anti-oxidant enzymes, such as an increase in cellular glutathione levels (GSH) and stress-induced activation of activator protein-1 (AP-1), play pivotal roles in the development of pathophysiology and degenerative disorders [>>58<<]. Another modulator, NO, a short-lived, lipophilic molecule, generated from L-arginine by various NADPH-dependent enzymes called NO synthases (NOSs) plays vital role in inducing cascades of pro-inflammatory molecules together with the
n3:mentions: n2:16934760

Subject Item: _:vb11323218
rdf:type: n3:Context
rdf:value: plays vital role in inducing cascades of pro-inflammatory molecules together with the physiologic functions such as vasodilatation, inhibition of platelet aggregation, neurotransmission, immune defence, and intracellular signalling [>>59<<]. NO is classified as a free radical species and some of its intermediates can damage DNA directly or interfere with DNA repair via protein damage [60,61].
n3:mentions: n2:11902565

Subject Item: _:vb11323219
rdf:type: n3:Context
rdf:value: NO is classified as a free radical species and some of its intermediates can damage DNA directly or interfere with DNA repair via protein damage [>>60<<,61]. Whereas high doses of NO (millimolar) seem to be cytotoxic and induce apoptosis, lower doses of NO (micro molar) can protect malignant cells from apoptosis in vitro through upregulation of COX-2 [62,63,64]. In addition, endothelial
n3:mentions: n2:7578935

Subject Item: _:vb11323220
rdf:type: n3:Context
rdf:value: NO is classified as a free radical species and some of its intermediates can damage DNA directly or interfere with DNA repair via protein damage [60,>>61<<]. Whereas high doses of NO (millimolar) seem to be cytotoxic and induce apoptosis, lower doses of NO (micro molar) can protect malignant cells from apoptosis in vitro through upregulation of COX-2 [62,63,64]. In addition, endothelial heme
n3:mentions: n2:8968069

Subject Item: _:vb11323221
rdf:type: n3:Context
rdf:value: Whereas high doses of NO (millimolar) seem to be cytotoxic and induce apoptosis, lower doses of NO (micro molar) can protect malignant cells from apoptosis in vitro through upregulation of COX-2 [>>62<<,63,64]. In addition, endothelial heme oxygenase-1 (HO-1) induced by cellular stress plays a critical role in defending the body against oxidant-induced injury during inflammatory processes [65].
n3:mentions: n2:9714315

Subject Item: _:vb11323222
rdf:type: n3:Context
rdf:value: Whereas high doses of NO (millimolar) seem to be cytotoxic and induce apoptosis, lower doses of NO (micro molar) can protect malignant cells from apoptosis in vitro through upregulation of COX-2 [62,>>63<<,64]. In addition, endothelial heme oxygenase-1 (HO-1) induced by cellular stress plays a critical role in defending the body against oxidant-induced injury during inflammatory processes [65].
n3:mentions: n2:9285487

Subject Item: _:vb11323223
rdf:type: n3:Context
rdf:value: Whereas high doses of NO (millimolar) seem to be cytotoxic and induce apoptosis, lower doses of NO (micro molar) can protect malignant cells from apoptosis in vitro through upregulation of COX-2 [62,63,>>64<<]. In addition, endothelial heme oxygenase-1 (HO-1) induced by cellular stress plays a critical role in defending the body against oxidant-induced injury during inflammatory processes [65].
n3:mentions: n2:9950682

Subject Item: _:vb11323224
rdf:type: n3:Context
rdf:value: In addition, endothelial heme oxygenase-1 (HO-1) induced by cellular stress plays a critical role in defending the body against oxidant-induced injury during inflammatory processes [>>65<<].
n3:mentions: n2:19016784

Subject Item: _:vb11323225
rdf:type: n3:Context
rdf:value: By the use of aspirin, a non-steroidal anti-inflammatory drug (NSAIDs), colon cancer risk can be reduced by 40%–50% by the COX-2 and COX-2 inhibition mechanism [>>66<<,67,68]. Another NASID, flurbiprofen, showed efficacy in inhibiting colon carcinogenesis due to its strong anti-metastatic effect together with the COX enzymes inhibition. Besides NSAIDs, the inhibitors of TNF-α, a highly studied
n3:mentions: n2:10774479

Subject Item: _:vb11323226
rdf:type: n3:Context
rdf:value: By the use of aspirin, a non-steroidal anti-inflammatory drug (NSAIDs), colon cancer risk can be reduced by 40%–50% by the COX-2 and COX-2 inhibition mechanism [66,>>67<<,68]. Another NASID, flurbiprofen, showed efficacy in inhibiting colon carcinogenesis due to its strong anti-metastatic effect together with the COX enzymes inhibition. Besides NSAIDs, the inhibitors of TNF-α, a highly studied
n3:mentions: n2:11138826

Subject Item: _:vb11323227
rdf:type: n3:Context
rdf:value: By the use of aspirin, a non-steroidal anti-inflammatory drug (NSAIDs), colon cancer risk can be reduced by 40%–50% by the COX-2 and COX-2 inhibition mechanism [66,67,>>68<<]. Another NASID, flurbiprofen, showed efficacy in inhibiting colon carcinogenesis due to its strong anti-metastatic effect together with the COX enzymes inhibition. Besides NSAIDs, the inhibitors of TNF-α, a highly studied
n3:mentions: n2:10630643

Subject Item: _:vb11323228
rdf:type: n3:Context
rdf:value: Besides NSAIDs, the inhibitors of TNF-α, a highly studied pro-inflammatory cytokines and immune cells modulators, have also been targeted as the way of treatment for various cancers in the current clinical trails [>>69<<]. Therefore, anti-inflammatory drugs might open additional therapeutic option for the treatment of cancers and other chronic diseases.
n3:mentions: n2:19277912

Subject Item: _:vb11323229
rdf:type: n3:Context
rdf:value: The generation of ROS, particularly O2− and OHֹ, play important roles in the development of cancer [>>54<<,55]. Therefore in order to prevent from the oxidative damage of DNA, lipid or protein the effects of these free radicals can be diluted by the anti-oxidant mechanism.
n3:mentions: n2:16563357

Subject Item: _:vb11323230
rdf:type: n3:Context
rdf:value: The generation of ROS, particularly O2− and OHֹ, play important roles in the development of cancer [54,>>55<<]. Therefore in order to prevent from the oxidative damage of DNA, lipid or protein the effects of these free radicals can be diluted by the anti-oxidant mechanism.
n3:mentions: n2:18089954

Subject Item: _:vb11323231
rdf:type: n3:Context
rdf:value: Curcumin at the concentration of 10 μM inhibited ROS generation in rat peritoneal macrophages [>>70<<]. Similar effects have been observed in red blood cells [71]. Curcumin has also been shown to scavenge O2− and OHֹ radicals [72,73].
n3:mentions: n2:7981240

Subject Item: _:vb11323232
rdf:type: n3:Context
rdf:value: Curcumin has also been shown to scavenge O2− and OHֹ radicals [72,>>73<<]. In contrary, a few reports showing curcumin as pro-oxidant indicated that the pro-oxidant and anti-oxidant effects of curcumin are dependent on dose and the chemical environment (e.g., availability of free Cu2+ ions) [74,75].
n3:mentions: n2:10418962

Subject Item: _:vb11323233
rdf:type: n3:Context
rdf:value: In contrary, a few reports showing curcumin as pro-oxidant indicated that the pro-oxidant and anti-oxidant effects of curcumin are dependent on dose and the chemical environment (e.g., availability of free Cu2+ ions) [74,>>75<<]. Another free radical, NO, also plays important roles as an oxidant, inflammatory- and immune-modulator. Preclinical studies have suggested that curcumin may inhibit induction of macrophage NOS activity at concentrations of 1–20 μM [76].
n3:mentions: n2:16109310

Subject Item: _:vb11323234
rdf:type: n3:Context
rdf:value: Preclinical studies have suggested that curcumin may inhibit induction of macrophage NOS activity at concentrations of 1–20 μM [>>76<<]. In mice, oral administration of an aqueous alkaline solution of curcumin, notably at a tiny dose of 92 ng/g-BW strongly inhibited murine hepatic lipopolysaccharide-induced iNOS gene expression [58]. As inhibition of iNOS activity may
n3:mentions: n2:7530002

Subject Item: _:vb11323235
rdf:type: n3:Context
rdf:value: In mice, oral administration of an aqueous alkaline solution of curcumin, notably at a tiny dose of 92 ng/g-BW strongly inhibited murine hepatic lipopolysaccharide-induced iNOS gene expression [>>58<<]. As inhibition of iNOS activity may represnt a mechanism of intervention during carcinogenesis, apparent activity of curcumin at low concentrations would have considerable implications for cancer chemoprevention.
n3:mentions: n2:16934760

Subject Item: _:vb11323236
rdf:type: n3:Context
rdf:value: in HO-1 mRNA, protein expression, and heme oxygenase enzymatic activity in bovine aortic endothelial cells and human proximal renal tubular cells at the concentration of 1–8 μM through the NF-κB pathways and transcriptional mechanisms [>>77<<]. Increased heme oxygenase activity also appears to play an important role in curcumin-mediated cytoprotection against oxidative stress and NO-induced toxicity or apoptosis [78].
n3:mentions: n2:11592943

Subject Item: _:vb11323237
rdf:type: n3:Context
rdf:value: Increased heme oxygenase activity also appears to play an important role in curcumin-mediated cytoprotection against oxidative stress and NO-induced toxicity or apoptosis [>>78<<].
n3:mentions: n2:10889462

Subject Item: _:vb11323238
rdf:type: n3:Context
rdf:value: shows anti-oxidant properties by providing hydrogen radicals and scavenging free radicals, there are a growing number of evidences that it can act as pro-oxidant under certain condition by generating ROS to show anticancer activity [>>79<<,80,81,82].
n3:mentions: n2:20944521

Subject Item: _:vb11323239
rdf:type: n3:Context
rdf:value: shows anti-oxidant properties by providing hydrogen radicals and scavenging free radicals, there are a growing number of evidences that it can act as pro-oxidant under certain condition by generating ROS to show anticancer activity [79,>>80<<,81,82]. The balance between anti-oxidant and pro-oxidant activity must be considered when planning intervention trials in healthy volunteers, particularly if pro-oxidant activity results in potentially damaging effects, as shown in
n3:mentions: n2:10456330

Subject Item: _:vb11323240
rdf:type: n3:Context
rdf:value: anti-oxidant properties by providing hydrogen radicals and scavenging free radicals, there are a growing number of evidences that it can act as pro-oxidant under certain condition by generating ROS to show anticancer activity [79,80,>>81<<,82]. The balance between anti-oxidant and pro-oxidant activity must be considered when planning intervention trials in healthy volunteers, particularly if pro-oxidant activity results in potentially damaging effects, as shown in
n3:mentions: n2:15700780

Subject Item: _:vb11323241
rdf:type: n3:Context
rdf:value: anti-oxidant properties by providing hydrogen radicals and scavenging free radicals, there are a growing number of evidences that it can act as pro-oxidant under certain condition by generating ROS to show anticancer activity [79,80,81,>>82<<]. The balance between anti-oxidant and pro-oxidant activity must be considered when planning intervention trials in healthy volunteers, particularly if pro-oxidant activity results in potentially damaging effects, as shown in biomarkers
n3:mentions: n2:12126798

Subject Item: _:vb11323242
rdf:type: n3:Context
rdf:value: pro-oxidant activity must be considered when planning intervention trials in healthy volunteers, particularly if pro-oxidant activity results in potentially damaging effects, as shown in biomarkers such as oxidative DNA adduct levels [>>83<<].
n3:mentions: n2:15790590

Subject Item: _:vb11323243
rdf:type: n3:Context
rdf:value: COX-2 is inducible at sites of inflammation by cytokines and intracellular signals; it can also be induced in various normal tissues by the hormones of ovulation and pregnancy, growth factors, oncogenes, and tumour promoters [>>84<<]. COX-2 is constitutively expressed only in brain and spinal cord tissue.
n3:mentions: n2:9811310

Subject Item: _:vb11323244
rdf:type: n3:Context
rdf:value: COX-2 over expression has been implicated in the carcinogenesis of many tumours such as in colon, rectum, breast, head and neck, lung, pancreas, stomach, and prostate [>>85<<].
n3:mentions: n2:11978897

Subject Item: _:vb11323245
rdf:type: n3:Context
rdf:value: It has been shown that curcumin is able to inhibit induction of COX-2 gene expression in oral and colon epithelial cells [>>86<<,87]. At a concentration of 20 μM, curcumin showed a strong inhibition of chemically induced PGE2 production in colon cells [40].
n3:mentions: n2:10190560

Subject Item: _:vb11323246
rdf:type: n3:Context
rdf:value: It has been shown that curcumin is able to inhibit induction of COX-2 gene expression in oral and colon epithelial cells [86,>>87<<]. At a concentration of 20 μM, curcumin showed a strong inhibition of chemically induced PGE2 production in colon cells [40].
n3:mentions: n2:16737669

Subject Item: _:vb11323247
rdf:type: n3:Context
rdf:value: At a concentration of 20 μM, curcumin showed a strong inhibition of chemically induced PGE2 production in colon cells [>>40<<]. In a study in human colon carcinoma cell lines carried by Lev-Ari et al., incubation of HT29 cells and SW480 cells with different concentrations of curcumin, resulted in inhibition of PGE2 synthesis, down regulation of COX-2 protein
n3:mentions: n2:7256789

Subject Item: _:vb11323248
rdf:type: n3:Context
rdf:value: HT29 cells and SW480 cells with different concentrations of curcumin, resulted in inhibition of PGE2 synthesis, down regulation of COX-2 protein levels, and increased apoptosis of those cells that constitutively express COX-2 protein [>>87<<]. One of the implicated mechanisms for COX-2 down regulation is inhibition of the activity of the IκK signalling complex responsible for phosphorylation of IκB and subsequently the activation of the transcription factor NF-κB [88].
n3:mentions: n2:16737669

Subject Item: _:vb11323249
rdf:type: n3:Context
rdf:value: One of the implicated mechanisms for COX-2 down regulation is inhibition of the activity of the IκK signalling complex responsible for phosphorylation of IκB and subsequently the activation of the transcription factor NF-κB [>>88<<]. This finding was also supported by the fact that commonly used anti-inflammatory drugs such as aspirin and salicylates, which inhibit the activity of IκB kinase-β, have also been linked to a decreased incidence of colorectal cancer [89].
n3:mentions: n2:10557090

Subject Item: _:vb11323250
rdf:type: n3:Context
rdf:value: This finding was also supported by the fact that commonly used anti-inflammatory drugs such as aspirin and salicylates, which inhibit the activity of IκB kinase-β, have also been linked to a decreased incidence of colorectal cancer [>>89<<].
n3:mentions: n2:9817203

Subject Item: _:vb11323251
rdf:type: n3:Context
rdf:value: Apart from the well known roles of COX-2 [>>84<<], later studies suggest that the COX-1 isozyme also plays role in inflammation and carcinogenesis; indeed the balance between the metabolic products of COX-1 and COX-2 catalysis appears important in physiologic function and response to
n3:mentions: n2:9811310

Subject Item: _:vb11323252
rdf:type: n3:Context
rdf:value: Curcumin and some of its analogues do appear to inhibit COX-1 transcription [>>88<<,90]. Such inhibition is important, as it has been linked to a potential influence on the local spread of malignancy and the communication between malignant cells and their neighbouring stromal cells [91,92].
n3:mentions: n2:10557090

Subject Item: _:vb11323253
rdf:type: n3:Context
rdf:value: Curcumin and some of its analogues do appear to inhibit COX-1 transcription [88,>>90<<]. Such inhibition is important, as it has been linked to a potential influence on the local spread of malignancy and the communication between malignant cells and their neighbouring stromal cells [91,92].
n3:mentions: n2:17202703

Subject Item: _:vb11323254
rdf:type: n3:Context
rdf:value: Such inhibition is important, as it has been linked to a potential influence on the local spread of malignancy and the communication between malignant cells and their neighbouring stromal cells [>>91<<,92].
n3:mentions: n2:16619535

Subject Item: _:vb11323255
rdf:type: n3:Context
rdf:value: Such inhibition is important, as it has been linked to a potential influence on the local spread of malignancy and the communication between malignant cells and their neighbouring stromal cells [91,>>92<<].
n3:mentions: n2:9630216

Subject Item: _:vb11323256
rdf:type: n3:Context
rdf:value: Numerous studies have indicated that the transcription factor, NF-κB plays important role to induce inflammation and is constitutively active in patients with cancer [>>93<<]. The role of NF-κB in suppression of apoptosis, tumour growth, invasion, angiogenesis, and metastasis, via a variety of downstream effectors, is well documented [94,95,96,97].
n3:mentions: n2:9918209

Subject Item: _:vb11323257
rdf:type: n3:Context
rdf:value: The role of NF-κB in suppression of apoptosis, tumour growth, invasion, angiogenesis, and metastasis, via a variety of downstream effectors, is well documented [>>94<<,95,96,97].
n3:mentions: n2:15380510

Subject Item: _:vb11323258
rdf:type: n3:Context
rdf:value: The role of NF-κB in suppression of apoptosis, tumour growth, invasion, angiogenesis, and metastasis, via a variety of downstream effectors, is well documented [94,>>95<<,96,97]. Therefore, an agent that can target NF-κB is of interest for the treatment of pancreatic cancer. From a philosophical standpoint, as cancer and most chronic diseases have a multifactor aetiology, natural diet-derived agents such
n3:mentions: n2:10485483

Subject Item: _:vb11323259
rdf:type: n3:Context
rdf:value: The role of NF-κB in suppression of apoptosis, tumour growth, invasion, angiogenesis, and metastasis, via a variety of downstream effectors, is well documented [94,95,>>96<<,97]. Therefore, an agent that can target NF-κB is of interest for the treatment of pancreatic cancer. From a philosophical standpoint, as cancer and most chronic diseases have a multifactor aetiology, natural diet-derived agents such as
n3:mentions: n2:10070951

Subject Item: _:vb11323260
rdf:type: n3:Context
rdf:value: The role of NF-κB in suppression of apoptosis, tumour growth, invasion, angiogenesis, and metastasis, via a variety of downstream effectors, is well documented [94,95,96,>>97<<]. Therefore, an agent that can target NF-κB is of interest for the treatment of pancreatic cancer. From a philosophical standpoint, as cancer and most chronic diseases have a multifactor aetiology, natural diet-derived agents such as
n3:mentions: n2:10657949

Subject Item: _:vb11323261
rdf:type: n3:Context
rdf:value: A pleiotropic activity in the cell is provided by ability of curcumin to inhibit multiple levels of the NF-κB, AP-1, and JNK signalling pathways [98,>>99<<,100].
n3:mentions: n2:9674701

Subject Item: _:vb11323262
rdf:type: n3:Context
rdf:value: A pleiotropic activity in the cell is provided by ability of curcumin to inhibit multiple levels of the NF-κB, AP-1, and JNK signalling pathways [98,99,>>100<<].
n3:mentions: n2:1905019

Subject Item: _:vb11323263
rdf:type: n3:Context
rdf:value: two diet-derived polyphenolic agents, the renoprotective and anti-oxidant properties of curcumin, in combination with the natural bioflavonoid quercetin, were tested in dialysis-dependent patients with cadaveric renal transplants [>>101<<]. It is known that the implicated mechanisms in renal graft rejection include alloimmune (T-cell-mediated cytotoxicity) and non-immune factors (e.g., cytomegalovirus infection, endothelial injury, and progressive atherosclerosis as a
n3:mentions: n2:16371925

Subject Item: _:vb11323264
rdf:type: n3:Context
rdf:value: mechanisms in renal graft rejection include alloimmune (T-cell-mediated cytotoxicity) and non-immune factors (e.g., cytomegalovirus infection, endothelial injury, and progressive atherosclerosis as a result of oxidative stress) [>>102<<,103]. In this study, both early graft and delayed graft functions were significantly improved in the drug (480 mg of curcumin and 20 mg of quercetin) treated group comparing to placebo group [101].
n3:mentions: n2:15954891

Subject Item: _:vb11323265
rdf:type: n3:Context
rdf:value: mechanisms in renal graft rejection include alloimmune (T-cell-mediated cytotoxicity) and non-immune factors (e.g., cytomegalovirus infection, endothelial injury, and progressive atherosclerosis as a result of oxidative stress) [102,>>103<<]. In this study, both early graft and delayed graft functions were significantly improved in the drug (480 mg of curcumin and 20 mg of quercetin) treated group comparing to placebo group [101].
n3:mentions: n2:8203375

Subject Item: _:vb11323266
rdf:type: n3:Context
rdf:value: In this study, both early graft and delayed graft functions were significantly improved in the drug (480 mg of curcumin and 20 mg of quercetin) treated group comparing to placebo group [>>101<<]. Another interesting observation was that tremor and neurotoxicity appeared to be less common in the drug treated group than in the control group. The investigators suggested that HO-1 induction may play a role in the improved early
n3:mentions: n2:16371925

Subject Item: _:vb11323267
rdf:type: n3:Context
rdf:value: The investigators suggested that HO-1 induction may play a role in the improved early outcomes of cadaveric renal recipients treated with curcumin and bioflavonoids [>>101<<,104].
n3:mentions: n2:16371925

Subject Item: _:vb11323268
rdf:type: n3:Context
rdf:value: The investigators suggested that HO-1 induction may play a role in the improved early outcomes of cadaveric renal recipients treated with curcumin and bioflavonoids [101,>>104<<].
n3:mentions: n2:11965035

Subject Item: _:vb11323269
rdf:type: n3:Context
rdf:value: Suppression of the inflammatory response by curcumin as discussed in the preclinical studies involves inhibition of the induction of COX-1, COX-2, iNOS, and production of cytokines such as interferon-γ [>>90<<,106]. It seems that many effects are achieved via suppression of the Janus kinase (JAK)-STAT signalling cascade via its effect on the Src homology 2 domain-containing protein tyrosine phosphatases (SHP)-2 [107].
n3:mentions: n2:17202703

Subject Item: _:vb11323270
rdf:type: n3:Context
rdf:value: Suppression of the inflammatory response by curcumin as discussed in the preclinical studies involves inhibition of the induction of COX-1, COX-2, iNOS, and production of cytokines such as interferon-γ [90,>>106<<]. It seems that many effects are achieved via suppression of the Janus kinase (JAK)-STAT signalling cascade via its effect on the Src homology 2 domain-containing protein tyrosine phosphatases (SHP)-2 [107].
n3:mentions: n2:12393461

Subject Item: _:vb11323271
rdf:type: n3:Context
rdf:value: It seems that many effects are achieved via suppression of the Janus kinase (JAK)-STAT signalling cascade via its effect on the Src homology 2 domain-containing protein tyrosine phosphatases (SHP)-2 [>>107<<]. In human multiple myeloma cells, curcumin has been shown to inhibit STAT3 phosphorylation and therefore to down regulate IL-6 production [44].
n3:mentions: n2:14634121

Subject Item: _:vb11323272
rdf:type: n3:Context
rdf:value: In human multiple myeloma cells, curcumin has been shown to inhibit STAT3 phosphorylation and therefore to down regulate IL-6 production [>>44<<].
n3:mentions: n2:11221833

Subject Item: _:vb11323273
rdf:type: n3:Context
rdf:value: In a pilot open-label study conducted in New York, oral curcumin was given to five patients with ulcerative proctitis and five patients with Crohn disease (CD) [>>108<<]. All the patients with proctitis noticed an improvement, and 80% of patients with CD showed better inflammatory profiles [108]. Subsequently, a randomized double-blind, placebo-controlled study was performed in patients with ulcerative
n3:mentions: n2:16240238

Subject Item: _:vb11323274
rdf:type: n3:Context
rdf:value: All the patients with proctitis noticed an improvement, and 80% of patients with CD showed better inflammatory profiles [>>108<<]. Subsequently, a randomized double-blind, placebo-controlled study was performed in patients with ulcerative colitis (UC) [109]. Of 89 patients enrolled, half received 1,000 mg of oral curcumin twice a day in combination with
n3:mentions: n2:16240238

Subject Item: _:vb11323275
rdf:type: n3:Context
rdf:value: Subsequently, a randomized double-blind, placebo-controlled study was performed in patients with ulcerative colitis (UC) [>>109<<]. Of 89 patients enrolled, half received 1,000 mg of oral curcumin twice a day in combination with sulfasalazine or mesalazine, two aminosalicylates that are standard treatments for UC, and the other half of the patients received an
n3:mentions: n2:17101300

Subject Item: _:vb11323276
rdf:type: n3:Context
rdf:value: The 6-month treatment schedule showed that patients in the curcumin group had a significantly reduced rate of relapse at six months (4.65% vs. 20.51% in the placebo group) [>>109<<].
n3:mentions: n2:17101300

Subject Item: _:vb11323277
rdf:type: n3:Context
rdf:value: In a study in postoperative patients, a significant anti-inflammatory effect was demonstrated in those receiving 400 mg of oral curcumin thrice daily for five days compared with placebo [>>110<<]. Using similar methods, considerable improvements in the patients’ symptoms were demonstrated in a double-blind study in India on patients with rheumatoid arthritis.
n3:mentions: n2:3546166

Subject Item: _:vb11323278
rdf:type: n3:Context
rdf:value: In this study, 1,200 mg of curcumin was administered four times daily to 18 patients with rheumatoid arthritis for two weeks, resulting in symptomatic improvement without apparent toxicity [>>27<<]. The anti-inflammatory properties of curcumin were demonstrated in two further studies examining the effects of oral curcumin on ophthalmologic diseases. In one of those, 375 mg of curcumin was given orally thrice daily to patients with
n3:mentions: n2:7390600

Subject Item: _:vb11323279
rdf:type: n3:Context
rdf:value: orally thrice daily to patients with chronic anterior uveitis for three months, resulting in a suggestion of improvement in the condition with comparable efficacy to that of steroids, which are generally regarded as standard treatment [>>111<<]. In a subsequent study by the same team, the same dose of curcumin (375 mg) was administered to eight patients with idiopathic inflammatory orbital pseudotumors for 6–22 months [112].
n3:mentions: n2:10404539

Subject Item: _:vb11323280
rdf:type: n3:Context
rdf:value: In a subsequent study by the same team, the same dose of curcumin (375 mg) was administered to eight patients with idiopathic inflammatory orbital pseudotumors for 6–22 months [>>112<<]. Half of the patients showed complete responses up to two years of follow-up. It is known that in patients with active psoriasis, increased activity of the enzyme phosphorylase kinase (PhK) mediates and triggers molecular mechanisms for
n3:mentions: n2:10960899

Subject Item: _:vb11323281
rdf:type: n3:Context
rdf:value: In an early preclinical study, Reddy and Aggarwal demonstrated that curcumin is a selective inhibitor of PhK [>>113<<]. More recently, PhK activity was assessed in 40 patients who were divided into four groups: a group of active untreated psoriasis, one of resolving psoriasis treated with calcipotriol [vitamin D3 analogue], a group of patients receiving
n3:mentions: n2:7511111

Subject Item: _:vb11323282
rdf:type: n3:Context
rdf:value: who were divided into four groups: a group of active untreated psoriasis, one of resolving psoriasis treated with calcipotriol [vitamin D3 analogue], a group of patients receiving curcumin, and a control group with healthy subjects [>>114<<]. This study showed that PhK activity was much higher in untreated patients, lower in the groups treated with calcipotriol and curcumin, and even lower in the control group.
n3:mentions: n2:11069500

Subject Item: _:vb11323283
rdf:type: n3:Context
rdf:value: and calcipotriol was associated with a suppression of keratinocyte transferrin receptor, the severity of parakeratosis, and the density of the epidermal cytotoxic CD8+ T cells, all considered clinical hallmarks of psoriatic activity [>>114<<].
n3:mentions: n2:11069500

Subject Item: _:vb11323284
rdf:type: n3:Context
rdf:value: In contrast to the systemic anti-oxidant properties of oral curcumin, it has been suggested that topical application of curcumin may result in increased formation of ROS in the skin when used in combination with other therapies [>>115<<]. Such potentially pro-oxidant effects may relate to dose or conditions, as discussed earlier.
n3:mentions: n2:16481714

Subject Item: _:vb11323285
rdf:type: n3:Context
rdf:value: In a study performed in Bradford, England, 15 Asian patients with acute vitiligo consumed turmeric daily and were treated with topical application of low-dose UVB-activated pseudocatalase (PC-KUS) for six months [>>115<<]. None of these patients showed any significant improvement of vitiligo. Eight patients were advised to stop turmeric consumption and continue with topical PC-KUS only twice daily. This led to a clinical improvement within two months and
n3:mentions: n2:16481714

Subject Item: _:vb11323286
rdf:type: n3:Context
rdf:value: No treatment-related toxicities were noticed [>>116<<].
n3:mentions: n2:11485087

Subject Item: _:vb11323287
rdf:type: n3:Context
rdf:value: et al. observed the reduced size of the lesions in 10 of the 62 patients receiving topical turmeric/curcumin in oral cancers and leukoplakia, however the report is lacking the control group and standard method of curcumin preparation [>>117<<].
n3:mentions: n2:2435036

Subject Item: _:vb11323288
rdf:type: n3:Context
rdf:value: A phase I clinical study performed in Taiwan investigated the potential anti-carcinogenesis activity of curcumin in patients with preinvasive malignant or high-risk premalignant conditions [>>28<<]. Twenty five patients with recently resected cancer of the bladder, Bowen disease of the skin, uterine cervical intraepithelial neoplasia, intestinal metaplasia of the stomach, or oral leukoplakia, were administered curcumin in doses of
n3:mentions: n2:11712783

Subject Item: _:vb11323289
rdf:type: n3:Context
rdf:value: Further evidence to support the hypothesis that curcumin has activity against preneoplastic lesions is provided by a recent study performed at The Cleveland Clinic in Florida in patients with familial adenomatous polyposis (FAP) [>>118<<]. FAP is an autosomal dominant condition characterized by the development of numerous bowel adenomas that can transform to adenocarcinoma.
n3:mentions: n2:16757216

Subject Item: _:vb11323290
rdf:type: n3:Context
rdf:value: All patients showed a decrease in the number and the size of polyps compared with baseline figures [>>118<<]. These preliminary data strongly support the case for designing a randomized controlled trial of curcumin versus standard therapy for patients with FAP.
n3:mentions: n2:16757216

Subject Item: _:vb11323291
rdf:type: n3:Context
rdf:value: In a Phase II clinical study report of Dhillon at el., twenty-five patients each treated with 8000 mg per day curcumin orally for two months observed peaked plasma curcumin level from 22 to 41 ng/mL [>>119<<]. On continuing up to 18 months, two patients showed clinical biological activity.
n3:mentions: n2:18628464

Subject Item: _:vb11323292
rdf:type: n3:Context
rdf:value: Recently, Goel et al. have discussed in details the effects of curcumin on various cancers in human [>>121<<] and Wilken et al. reviewed the mechanism of anti-cancer properties of curcumin focused on head and neck squamous cell carcinoma [122].
n3:mentions: n2:20924967

Subject Item: _:vb11323293
rdf:type: n3:Context
rdf:value: Recently, Goel et al. have discussed in details the effects of curcumin on various cancers in human [121] and Wilken et al. reviewed the mechanism of anti-cancer properties of curcumin focused on head and neck squamous cell carcinoma [>>122<<]. Both reviews provide additional information on molecular mechanism of anticancer effects on curcumin.
n3:mentions: n2:21299897

Subject Item: _:vb11323294
rdf:type: n6:Section
dc:title: recent advancements on curcumin formulations and delivery systems
n6:contains: _:vb11323295 _:vb11323324 _:vb11323325 _:vb11323326 _:vb11323320 _:vb11323321 _:vb11323322 _:vb11323323 _:vb11323316 _:vb11323317 _:vb11323318 _:vb11323319 _:vb11323312 _:vb11323313 _:vb11323314 _:vb11323315 _:vb11323308 _:vb11323309 _:vb11323310 _:vb11323311 _:vb11323304 _:vb11323305 _:vb11323306 _:vb11323307 _:vb11323300 _:vb11323301 _:vb11323302 _:vb11323303 _:vb11323296 _:vb11323297 _:vb11323298 _:vb11323299

Subject Item: _:vb11323295
rdf:type: n3:Context
rdf:value: It is well established fact that the main limitation of broader use of curcumin-based formulations is its poor solubility and fast metabolism [>>123<<]. Therefore, in order to increase its solubility, stability and pharmacological activities, further research on improved formulations and delivery systems is needed to achieve its optimum therapeutic effects. In this section some recent
n3:mentions: n2:21311958

Subject Item: _:vb11323296
rdf:type: n3:Context
rdf:value: Kurien et al. claimed that the solubility of curcumin and turmeric can be increased by 12-fold and 3-fold, respectively, by the use of heat without heat-mediated disintegration of curcumin [>>124<<]. For delivery of drugs in vivo, water is indisputably the simplest and the safest vehicle, therefore possibility of considering heat-solubilized curcumin for future in vivo and in vitro studies might be interesting [124]. Zebib et al.
n3:mentions: n2:19618459

Subject Item: _:vb11323297
rdf:type: n3:Context
rdf:value: For delivery of drugs in vivo, water is indisputably the simplest and the safest vehicle, therefore possibility of considering heat-solubilized curcumin for future in vivo and in vitro studies might be interesting [>>124<<]. Zebib et al. prepared complexes of curcumin with metal ions (Zn2+, Cu2+, Mg2+ and Se2+) that were found to be readily soluble in water-glycerol (1:1; w/w) and quite stable towards light and heat [125]. Complexes of curcumin with serum
n3:mentions: n2:19618459

Subject Item: _:vb11323298
rdf:type: n3:Context
rdf:value: Qiu et al. reported chemically modified 4-arylidene curcumin derivatives that were found to be more soluble and more potent anti-cancer targeted analogues [>>127<<]. In addition, several attempts have also been made to prepare chemically modified curcumin in order to increase its activity against cancer and NF-κB [128,129,130,131,132,133]. Safavy et al. developed water-soluble curcumin conjugates
n3:mentions: n2:21070043

Subject Item: _:vb11323299
rdf:type: n3:Context
rdf:value: In addition, several attempts have also been made to prepare chemically modified curcumin in order to increase its activity against cancer and NF-κB [>>128<<,129,130,131,132,133].
n3:mentions: n2:12408714

Subject Item: _:vb11323300
rdf:type: n3:Context
rdf:value: In addition, several attempts have also been made to prepare chemically modified curcumin in order to increase its activity against cancer and NF-κB [128,>>129<<,130,131,132,133].
n3:mentions: n2:16789753

Subject Item: _:vb11323301
rdf:type: n3:Context
rdf:value: In addition, several attempts have also been made to prepare chemically modified curcumin in order to increase its activity against cancer and NF-κB [128,129,>>130<<,131,132,133].
n3:mentions: n2:16843665

Subject Item: _:vb11323302
rdf:type: n3:Context
rdf:value: In addition, several attempts have also been made to prepare chemically modified curcumin in order to increase its activity against cancer and NF-κB [128,129,130,>>131<<,132,133]. Safavy et al. developed water-soluble curcumin conjugates with two differently sized poly(ethyleneglycol) molecules. The soluble conjugates exhibited enhanced cytotoxicity as compared to curcumin alone and showed potentials in
n3:mentions: n2:16338138

Subject Item: _:vb11323303
rdf:type: n3:Context
rdf:value: In addition, several attempts have also been made to prepare chemically modified curcumin in order to increase its activity against cancer and NF-κB [128,129,130,131,>>132<<,133]. Safavy et al. developed water-soluble curcumin conjugates with two differently sized poly(ethyleneglycol) molecules. The soluble conjugates exhibited enhanced cytotoxicity as compared to curcumin alone and showed potentials in
n3:mentions: n2:15210154

Subject Item: _:vb11323304
rdf:type: n3:Context
rdf:value: The soluble conjugates exhibited enhanced cytotoxicity as compared to curcumin alone and showed potentials in anti-cancer treatment [>>134<<].
n3:mentions: n2:17973470

Subject Item: _:vb11323305
rdf:type: n3:Context
rdf:value: The study confirmed the potential of polymeric implants to avoid oral route and provide sustained release of incorporated curcumin [>>123<<].
n3:mentions: n2:21311958

Subject Item: _:vb11323306
rdf:type: n3:Context
rdf:value: Moreover, micelles decreased curcumin uptake by liver and spleen, and at the same time, enhanced distribution of curcumin in lung and brain [>>136<<].
n3:mentions: n2:21044788

Subject Item: _:vb11323307
rdf:type: n3:Context
rdf:value: The in vivo pharmacokinetics revealed that nanoparticles-incorportaed curcumin achieved a 9-fold increase in oral bioavailability as compared to curcumin administered with piperine as absorption enhancer [>>137<<]. Tsai et al. prepared an optimized polylactic-co-glycolic acid (PLGA) nano-formulation of curcumin which resulted in a 22-fold higher oral bioavailability in rats as compared to conventional curcumin [138]. Curcumin loaded dextran
n3:mentions: n2:19491009

Subject Item: _:vb11323308
rdf:type: n3:Context
rdf:value: Tsai et al. prepared an optimized polylactic-co-glycolic acid (PLGA) nano-formulation of curcumin which resulted in a 22-fold higher oral bioavailability in rats as compared to conventional curcumin [>>138<<]. Curcumin loaded dextran sulphate-chitosan nanoparticles showed preferential killing of cancer cells compared to normal cells, indicating potential in targeting [139].
n3:mentions: n2:25214079

Subject Item: _:vb11323309
rdf:type: n3:Context
rdf:value: It remains to be seen whether the same nanocurcumin will display enhanced anti-cancer activity as well [>>141<<]. A similar approach in reducing the size of curcumin crystals was proposed by Gao et al. to produce nanosupsensions for intravenous delivery [142].
n3:mentions: n2:21322563

Subject Item: _:vb11323310
rdf:type: n3:Context
rdf:value: A similar approach in reducing the size of curcumin crystals was proposed by Gao et al. to produce nanosupsensions for intravenous delivery [>>142<<].
n3:mentions: n2:20939679

Subject Item: _:vb11323311
rdf:type: n3:Context
rdf:value: Wu et al. developed water-dispersible hybrid nanogels for intracellular delivery of curcumin aiming at photodermal therapy [>>143<<]. The hybrid combines optical label (Au/Ag bimetallic nanoparticle, polystyrene gel layer, polyethylene gel and provides potent cytotoxicity against B16F10 cells by combined chemo-phototermal treatment.
n3:mentions: n2:20933280

Subject Item: _:vb11323312
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rdf:value: In comparison, Tween-based formulations failed to achieve the same effect [>>144<<].
n3:mentions: n2:26059118

Subject Item: _:vb11323313
rdf:type: n3:Context
rdf:value: Complexation of curcumin with phosphatidylcholine resulted in enhanced bioavailability, improved pharmacokinetics and increased hepatoprotective activity as compared to physical mixtures of curcumin and phosphatidylcholine [>>145<<]. Curcumin formulated with Meriva® (phosphatidylcholine) showed increased bioavailability in rats [146]. Curcumin-phospholipid complex administered orally resulted in higher serum concentrations of curcumin as compared to uncomplexed
n3:mentions: n2:21374628

Subject Item: _:vb11323314
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rdf:value: Curcumin formulated with Meriva® (phosphatidylcholine) showed increased bioavailability in rats [>>146<<]. Curcumin-phospholipid complex administered orally resulted in higher serum concentrations of curcumin as compared to uncomplexed curcumin. Moreover, the complex maintained the effective concentrations of curcumin over longer period of
n3:mentions: n2:17051370

Subject Item: _:vb11323315
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rdf:value: Moreover, the complex maintained the effective concentrations of curcumin over longer period of time [>>147<<]. However, the content of curcumin in complexes was found to be limited to about 17 and 32% (w/w), respectively, which is much lower than what could be achieved by liposomal encapsulation of curcumin.
n3:mentions: n2:17112692

Subject Item: _:vb11323316
rdf:type: n3:Context
rdf:value: Phospholipid vesicles and lipid-nanospheres embedding curcumin improved intravenous delivery of curcumin to tissue macrophages, especially bone marrow and spleen macrophages [>>148<<]. Solid lipid nanoparticles (SLN) were also proposed as mean to enhance oral bioavailability of curcumin.
n3:mentions: n2:18063327

Subject Item: _:vb11323317
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rdf:value: Pharmacokinetic profile of curcumin on SLN in rats showed significant improvement as compared to solubilized curcumin [>>149<<]. In order to further enhance anti-cancer potential of curcumin, transferrin-mediated SLN containing curcumin were developed and their superiority confirmed in breast cancer cells [150]. Solid lipid nanoparticles were proposed for topical
n3:mentions: n2:20938993

Subject Item: _:vb11323318
rdf:type: n3:Context
rdf:value: In order to further enhance anti-cancer potential of curcumin, transferrin-mediated SLN containing curcumin were developed and their superiority confirmed in breast cancer cells [>>150<<]. Solid lipid nanoparticles were proposed for topical application of curcumin as well [151]. Solid lipid nanoparticles developed by Yadav et al., were evaluated in rat model of inflammatory bowel disease and showed enhanced
n3:mentions: n2:20655375

Subject Item: _:vb11323319
rdf:type: n3:Context
rdf:value: Solid lipid nanoparticles were proposed for topical application of curcumin as well [>>151<<]. Solid lipid nanoparticles developed by Yadav et al., were evaluated in rat model of inflammatory bowel disease and showed enhanced anti-angiogenic and anti-inflammatory activities [152].
n3:mentions: n2:17287099

Subject Item: _:vb11323320
rdf:type: n3:Context
rdf:value: Solid lipid nanoparticles developed by Yadav et al., were evaluated in rat model of inflammatory bowel disease and showed enhanced anti-angiogenic and anti-inflammatory activities [>>152<<].
n3:mentions: n2:19222903

Subject Item: _:vb11323321
rdf:type: n3:Context
rdf:value: anti-angiogenesis effects were suppressed in vivo and based on their results the authors propose that liposomal curcumin for systemic delivery provides the rationale for the treatment of patients suffering from pancreatic carcinoma [>>156<<]. Li et al. developed liposomal curcumin which showed dose-dependent growth inhibition and apoptosis in the two human colorectal cancer cell lines (LoVo and Colo205 cells) and synergetic effect with oxaliplatin, a standard chemotherapy
n3:mentions: n2:16092118

Subject Item: _:vb11323322
rdf:type: n3:Context
rdf:value: In in vivo study, liposomal curcumin significantly inhibited tumour growth in Colo205 and LoVo xenografts in mice [>>157<<]. Thangapazham et al. developed liposomal delivery system for curcumin in which liposomes were coated with prostate membrane specific antigen specific antibodies to achieve targeting. The superiority of such a system was evaluated in two
n3:mentions: n2:17431105

Subject Item: _:vb11323323
rdf:type: n3:Context
rdf:value: It was also observed that LNCaP cells were relatively more sensitive to liposomal curcumin than C4-2B cells [>>158<<]. Wang et al. reported on liposomal formulation of curcumin able to suppress the growth of head and neck squamous cell carcinoma (HNSCC) in in vitro study in dose-dependent manner and also able to suppress the activation of NF-κB without
n3:mentions: n2:18425340

Subject Item: _:vb11323324
rdf:type: n3:Context
rdf:value: The authors speculated that liposomal curcumin is a viable non-toxic therapeutic agent for HNSCC [>>159<<]. Takahashi et al. developed liposomal delivery system for oral administration of curcumin, incorporating up to 68% of curcumin. Faster rate and better absorption after oral administration in rats where achieved as compared to
n3:mentions: n2:18829502

Subject Item: _:vb11323325
rdf:type: n3:Context
rdf:value: These findings suggested that liposomal phytochemicals-in-combination may reduce prostate cancer incidence [>>162<<]. Mourtas et al. proposed novel curcumin-decorated nanoliposomes with very high affinity for amyloid-β-42 peptide as vectors for targeted delivery of Alzheimer disease treatment. This approach opens the possibility to further explore the
n3:mentions: n2:19326431

Subject Item: _:vb11323326
rdf:type: n3:Context
rdf:value: This approach opens the possibility to further explore the potential of vesicle-surface available curcumin in various cancer treatments [>>163<<].
n3:mentions: n2:21131044

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