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n7:10.1371%2Fjournal.pone.0012969 n9:0 n10:0 n11:20885979
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10.1371%2Fjournal.pone.0012969
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introduction
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Clinical and lab researches showed that variety of factors could weaken or undermine the intestinal barrier structure and function, such as trauma, sepsis[>>1<<], operation, chemotherapy, radiotherapy, severe pancreatitis, long-term parenteral nutrition, and so on, thus resulted in bacteria translocation, subsequently led to endogenous infection and endotoxiemia (ETM).
n2:mentions
n3:8703632
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The final consequence of IMBdysfunction is systemic inflammation response syndrome (SIRS) and multiple organs dysfunction syndrome (MODS) [>>2<<]. Intestine is considered to be not only the target organ of MODS, but also the initiator of MODS. Therefore, IMB function has become an important prognostic indicator for critically ill patients [3].
n2:mentions
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Therefore, IMB function has become an important prognostic indicator for critically ill patients [>>3<<].
n2:mentions
n3:10889150
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Examination of D-lactate in peripheral blood can evaluate damage situation of intestinal mucosa because of lack of D-lactate dehydrogenase in mammals [>>4<<]. The other indicator is Diamine oxidase (DAO), one kind of endocellular enzyme, only exists in villus cytoplasm of intestinal stratum supravasculare in mammals. When intestinal epithelial cells are injured, endocellular DAO released into
n2:mentions
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Hence, the activity of DAO in blood indicates maturity and integrity of intestinal mucosa [>>5<<]. Above all, the evaluation of IMB function is depended on these two indicators in our research.
n2:mentions
n3:11052326
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Based on an accurate assessment of IMB function, here, we intend to find a proper drug capable for protecting it, and thus for prevention and treatment of intestinal inflammation [>>6<<]–[8]. In recent years, researchers focused on the traditional Chinese medicine for its better therapeutic effects and less toxic side effects.
n2:mentions
n3:15139492
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Based on an accurate assessment of IMB function, here, we intend to find a proper drug capable for protecting it, and thus for prevention and treatment of intestinal inflammation [6]–[>>8<<]. In recent years, researchers focused on the traditional Chinese medicine for its better therapeutic effects and less toxic side effects.
n2:mentions
n3:15065005
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Curcumin,isolated from the rhizomes of the plant Curcuma longa Linn, has anti-inflammation, anti-oxidization and free radical removal effects [>>9<<]. Tremendous research papers have reported intriguing pharmacologic effects associated with curcumin. It can attenuate experimental colitis by inhibiting the activation of NF-κB and reducing the activity of p38 MAPK[10]–[12]. Curcumin can
n2:mentions
n3:17158101
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It can attenuate experimental colitis by inhibiting the activation of NF-κB and reducing the activity of p38 MAPK[>>10<<]–[12]. Curcumin can also suppress the activation of NF-κB in ethanol-induced liver injury in rats [13]. The previous research showed that the inhibition of inhibitory factor I-κB kinase activity is a possible mechanism by which curcumin
n2:mentions
n3:17276891
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It can attenuate experimental colitis by inhibiting the activation of NF-κB and reducing the activity of p38 MAPK[10]–[>>12<<]. Curcumin can also suppress the activation of NF-κB in ethanol-induced liver injury in rats [13]. The previous research showed that the inhibition of inhibitory factor I-κB kinase activity is a possible mechanism by which curcumin blocks
n2:mentions
n3:12454848
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Curcumin can also suppress the activation of NF-κB in ethanol-induced liver injury in rats [>>13<<]. The previous research showed that the inhibition of inhibitory factor I-κB kinase activity is a possible mechanism by which curcumin blocks NF-κB activation [14]. Moreover, curcumin was proved to suppress the p38, JNK and NF-κB p65 in
n2:mentions
n3:18209571
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The previous research showed that the inhibition of inhibitory factor I-κB kinase activity is a possible mechanism by which curcumin blocks NF-κB activation [>>14<<]. Moreover, curcumin was proved to suppress the p38, JNK and NF-κB p65 in human intestinal epithelial HT29 cell line. Curcumin also attenuated Stx-1 induced cell death [15]. Hence, the evidences from the studies both in vitro and in vivo
n2:mentions
n3:10477620
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Curcumin also attenuated Stx-1 induced cell death [>>15<<]. Hence, the evidences from the studies both in vitro and in vivo indicated that curcumin acted as a protective reagent against inflammation or infection.
n2:mentions
n3:10531258
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results
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MKP-1, one of the dephosphorylated factors of MAPK, which can inhibit the activity of ERK, JNK and p38 in stress reaction[>>22<<], [23], participates in regulation of multiple physiological and pathological processes, including inflammatory reaction by regulating the activity of ERK, JNK and p38.
n2:mentions
n3:15722358
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MKP-1, one of the dephosphorylated factors of MAPK, which can inhibit the activity of ERK, JNK and p38 in stress reaction[22], [>>23<<], participates in regulation of multiple physiological and pathological processes, including inflammatory reaction by regulating the activity of ERK, JNK and p38.
n2:mentions
n3:10678585
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Beside MAPK signal pathway, NF-κB pathway is the most important downstream signal transduction pathway mediated by LPS [>>24<<]–[27]. Some studies have shown that activation of MAPK phosphorylation transduction signals could activate downstream transcription of NF-κB-mediated pro-inflammatory cytokines.
n2:mentions
n3:15265936
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Beside MAPK signal pathway, NF-κB pathway is the most important downstream signal transduction pathway mediated by LPS [24]–[>>27<<]. Some studies have shown that activation of MAPK phosphorylation transduction signals could activate downstream transcription of NF-κB-mediated pro-inflammatory cytokines.
n2:mentions
n3:18164817
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dc:title
methods
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Enteritis was induced in rats through peritoneal injection of MTX (20 mg/kg) [>>16<<]. Rats were randomly divided into 4 groups:
n2:mentions
n3:12613655
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DAI were evaluated based on the general symptoms of rats during the disease progress including weight decent percentage, stool viscidity and bloody stools according to the scoring system [>>17<<]. On the 7th day animal models were made, the rats were killed, and the intestinal segments of rats were observed with unaided eye to determine the CMDI [18].
n2:mentions
n3:10958782
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On the 7th day animal models were made, the rats were killed, and the intestinal segments of rats were observed with unaided eye to determine the CMDI [>>18<<]. Severity of colitis was graded on a scale of 0–IV and defined as the pathological index according to the standard scoring system [19]. Finally, the intestinal mucosa samples were fixed in 10% formaldehyde solution at room temperature
n2:mentions
n3:12617886
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Severity of colitis was graded on a scale of 0–IV and defined as the pathological index according to the standard scoring system [>>19<<]. Finally, the intestinal mucosa samples were fixed in 10% formaldehyde solution at room temperature according to standard method. Briefly, samples were embedded in paraffin, then sectioned at 5 µm, and stained with Hematoxylin-Eosin,
n2:mentions
n3:10732770
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All samples were evaluated and by an experienced pathologist who is blinded to the experiment. Finally, we got histological score (HS) for each samples [>>20<<].
n2:mentions
n3:12702039
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After the plasma was deproteined with perchloric acid, the levels of D-lactate and DAO in the serum were detected by spectrophotometry as the same method described in reference lectures [>>12<<], [17].
n2:mentions
n3:12454848
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After the plasma was deproteined with perchloric acid, the levels of D-lactate and DAO in the serum were detected by spectrophotometry as the same method described in reference lectures [12], [>>17<<].
n2:mentions
n3:10958782
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Nuclear extracts were prepared as described previously [>>21<<]. Use NF-κB activation-translocation detection kit to detect the location of NF-κB, according to the manufacturer's instructions.
n2:mentions
n3:14744935
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_:vb8862790
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discussion
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structural damage is as follows: intestinal mucosa cells release chemokine and cytokines after stimulated by causative factors; inflammatory cells infiltrate and release inflammatory mediators; finally lead to cell death or apoptosis [>>28<<]. Leukocyte's over-activation is a very important knot of this process. The level of MPO, an enzyme mainly existing in neutrophil, reflects the level of neutrophil infiltration.
n2:mentions
n3:12057768
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Moreover, ICAM-1, belonging to the immunoglobulin superfamily, has received the attention in recent years in the process of IBD[29]–[>>30<<]. Our data showed that the mRNA expression of ICAM-1 was significantly suppressed by curcumin in vitro and in vivo (Fig. 3B and C). All of this results suggested that curcumin played anti-inflammatory role partly by inhibiting neutrophil
n2:mentions
n3:18325348
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It also served as the mediator for intestinal mucosa injury[>>31<<]–[33]. TNF-α participates in early steps of inflammation, causes aggregation of inflammatory cells and plays important roles in inducting expression of other inflammatory cytokines[34].
n2:mentions
n3:7634977
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On the other hand, IL-10, identified as an anti-inflammatory cytokine, suppresses T lymphocytes and mononuclear cell function and many pro-inflammatory cytokines [>>35<<]–[37]. We detected the level of IL-10 by ELISA, and discovered that it was up-regulated by curcumin in vivo and in vitro (Fig. 5A and B). Curcumin down-regulated pro-inflammatory cytokine expression, while up-regulated anti-inflammatory
n2:mentions
n3:17855067
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On the other hand, IL-10, identified as an anti-inflammatory cytokine, suppresses T lymphocytes and mononuclear cell function and many pro-inflammatory cytokines [35]–[>>37<<]. We detected the level of IL-10 by ELISA, and discovered that it was up-regulated by curcumin in vivo and in vitro (Fig. 5A and B). Curcumin down-regulated pro-inflammatory cytokine expression, while up-regulated anti-inflammatory
n2:mentions
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Additionally, reactive oxygen species (ROS) plays a “trigger” role in the pathophysiological process of intestinal structural damage [>>38<<]–[40]. We tested curcumin for its ability to inhibit the combined inflammatory and oxidative damage which occured as a response to inflammatory in the enteritis rat models.
n2:mentions
n3:3020994
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Additionally, reactive oxygen species (ROS) plays a “trigger” role in the pathophysiological process of intestinal structural damage [38]–[>>40<<]. We tested curcumin for its ability to inhibit the combined inflammatory and oxidative damage which occured as a response to inflammatory in the enteritis rat models.
n2:mentions
n3:9744694
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have proved that anti-oxidant function of intestinal mucosa was damaged in the animal model of salmonella infection, chronic diarrhea and ulcerative colitis, and oxygen free radical scavenger could be used to treat such diseases [>>41<<]–[43]. The anti-oxidant defense system in the intestinal mucosa for eliminating ROS, contains enzymes system and non-enzymes system.
n2:mentions
n3:10889150
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have proved that anti-oxidant function of intestinal mucosa was damaged in the animal model of salmonella infection, chronic diarrhea and ulcerative colitis, and oxygen free radical scavenger could be used to treat such diseases [41]–[>>43<<]. The anti-oxidant defense system in the intestinal mucosa for eliminating ROS, contains enzymes system and non-enzymes system.
n2:mentions
n3:6406546
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Accumulating evidence supported that intestinal injury, including ischemic, inflammation, apoptosis and other pathological mechanisms were related with the regulation of MAPK [>>20<<] and NF-κB signal pathway [15], [21], [44]–[50].
n2:mentions
n3:12702039
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Accumulating evidence supported that intestinal injury, including ischemic, inflammation, apoptosis and other pathological mechanisms were related with the regulation of MAPK [20] and NF-κB signal pathway [>>15<<], [21], [44]–[50].
n2:mentions
n3:10531258
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Accumulating evidence supported that intestinal injury, including ischemic, inflammation, apoptosis and other pathological mechanisms were related with the regulation of MAPK [20] and NF-κB signal pathway [15], [>>21<<], [44]–[50].
n2:mentions
n3:14744935
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Accumulating evidence supported that intestinal injury, including ischemic, inflammation, apoptosis and other pathological mechanisms were related with the regulation of MAPK [20] and NF-κB signal pathway [15], [21], [>>44<<]–[50]. The expression of IL-10 is under the control of the Sp1 transcription factor that is also regulated by MAPK pathway [51]. Therefore, we disscused the role of curcumin on two pathways. MAPK which consists of three major subgroups,
n2:mentions
n3:17186389
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Accumulating evidence supported that intestinal injury, including ischemic, inflammation, apoptosis and other pathological mechanisms were related with the regulation of MAPK [20] and NF-κB signal pathway [15], [21], [44]–[>>50<<]. The expression of IL-10 is under the control of the Sp1 transcription factor that is also regulated by MAPK pathway [51]. Therefore, we disscused the role of curcumin on two pathways. MAPK which consists of three major subgroups, ERK1/2,
n2:mentions
n3:11994493
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The expression of IL-10 is under the control of the Sp1 transcription factor that is also regulated by MAPK pathway [>>51<<]. Therefore, we disscused the role of curcumin on two pathways. MAPK which consists of three major subgroups, ERK1/2, JNK1/2 and p38 MAPK plays a key role in transducing various extracellular signals to nucleus and regulating cell growth
n2:mentions
n3:17916230
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Moreover, MAPK takes part in the LPS-mediated signal transduction pathway [>>52<<]–[54] and controls cellular responses to cytokines and stressors.
n2:mentions
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Moreover, MAPK takes part in the LPS-mediated signal transduction pathway [52]–[>>54<<] and controls cellular responses to cytokines and stressors.
n2:mentions
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MKP-1, another special MAPK family, is capable of dephosphorylating and inactivating various members of the MAPK family [55], [>>56<<]. It is reported that MKP-1 deficiency enhanced phosphorylation of p38 and JNK [57].
n2:mentions
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NF-κB activation enhances the transcription of pro-inflammatory cytokines, and the cytokines are known to in-turn activate NF-κB [>>58<<]. Thus we still detected whether curcumin could regulat NF-κB signal pathway. NF-κB is located in cytoplasm and bounds to I-κB as an inactive complex. The phosphorylation and subsequent degradation of I-κB result in separation of the
n2:mentions
n3:8782457
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The activated NF-κB migrates into the nucleus, and causes the expression of inflammatory cytokines, such as TNF-α, IL-6 and IL-8 [>>59<<]. Meanwhile, NF-κB can be activated by inflammatory factors such as IL-1β and TNF-α [60]. In addition NF-κB signaling pathway is the downstream pathway of LPS-mediated transduction pathways. Here, we displayed the level of I-κB was
n2:mentions
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Meanwhile, NF-κB can be activated by inflammatory factors such as IL-1β and TNF-α [>>60<<]. In addition NF-κB signaling pathway is the downstream pathway of LPS-mediated transduction pathways. Here, we displayed the level of I-κB was degradated in MTX-induced rat intestinal mucosa and LPS-treated IEC-6 cells, while it was
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