Quercetin attenuates the ischemia reperfusion induced COX-2 and MPO expression in the small intestine mucosa

2017 ◽  
Vol 95 ◽  
pp. 346-354 ◽  
Author(s):  
Štefan Tóth ◽  
Zuzana Jonecová ◽  
Kristína Čurgali ◽  
Milan Maretta ◽  
Ján Šoltés ◽  
...  
Keyword(s):  
Small Intestine ◽  
Ischemia Reperfusion ◽  
Intestine Mucosa ◽  
Cox 2

Activation of the MyD88 signaling pathway inhibits ischemia-reperfusion injury in the small intestine

2012 ◽  
Vol 303 (3) ◽  
pp. G324-G334 ◽  
Author(s):  
Toshio Watanabe ◽  
Atsushi Kobata ◽  
Tetsuya Tanigawa ◽  
Yuji Nadatani ◽  
Hirokazu Yamagami ◽  
...  
Keyword(s):  
Small Intestine ◽  
Signaling Pathway ◽  
Knockout Mice ◽  
Ischemia Reperfusion ◽  
Adaptor Protein ◽  
Myeloperoxidase Activity ◽  
Wild Type ◽  
Tnf Α ◽  
Cox 2 ◽  
Myd88 Signaling

Toll-like receptors (TLRs) recognize microbial components and trigger the signaling cascade that activates innate and adaptive immunity. Recent studies have shown that the activation of TLR-dependent signaling pathways plays important roles in the pathogenesis of ischemia-reperfusion (I/R) injuries in many organs. All TLRs, except TLR3, use a common adaptor protein, MyD88, to transduce activation signals. We investigated the role of MyD88 in I/R injury of the small intestine. MyD88 and cyclooxygenase-2 (COX-2) knockout and wild-type mice were subjected to intestinal I/R injury. I/R-induced small intestinal injury was characterized by infiltration of inflammatory cells, disruption of the mucosal epithelium, destruction of villi, and increases in myeloperoxidase activity and mRNA levels of TNF-α and the IL-8 homolog KC. MyD88 deficiency worsened the severity of I/R injury, as assessed using the histological grading system, measuring luminal contents of hemoglobin (a marker of intestinal bleeding), and counting apoptotic epithelial cells, while it inhibited the increase in mRNA expression of TNF-α and KC. I/R significantly enhanced COX-2 expression and increased PGE2 concentration in the small intestine of wild-type mice, which were markedly inhibited by MyD88 deficiency. COX-2 knockout mice were also highly susceptible to intestinal I/R injury. Exogenous PGE2 reduced the severity of injury in both MyD88 and COX-2 knockout mice to the level of wild-type mice. These findings suggest that the MyD88 signaling pathway may inhibit I/R injury in the small intestine by inducing COX-2 expression.

Granulocyte accumulation in postischemic intestine: role of leukocyte adhesion glycoprotein CD11/CD18

1992 ◽  
Vol 262 (5) ◽  
pp. G878-G882 ◽  
Author(s):  
H. Kurtel ◽  
P. Tso ◽  
D. N. Granger
Keyword(s):  
Small Intestine ◽  
Bowel Wall ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
Neutrophil Infiltration ◽  
Myeloperoxidase Activity ◽  
Specific Monoclonal Antibody ◽  
Neutrophil Accumulation ◽  
Intestine Mucosa

Neutrophils play an important role in ischemia-reperfusion (I/R)-induced vascular injury in the small intestine. Monoclonal antibodies against the leukocyte adhesion glycoprotein CD11/CD18 afford protection against I/R-induced microvascular injury. It has been suggested that the response to I/R differs between the various layers of the bowel wall, with relatively few granulocytes accumulating in the mucosa compared with the serosa or mesentery. The objectives of this study were to determine whether I/R-induced neutrophil accumulation is 1) homogenous in the different layers of intestine (mucosa, submucosa, muscle, and mesentery) and 2) dependent on the expression and/or activation of the leukocyte adhesion glycoprotein CD11/CD18. Neutrophil infiltration was monitored by measuring myeloperoxidase activity in mucosa, submucosa, muscle, and mesentery of cat small intestine subjected to 3 h ischemia (blood flow reduced to 20% of control) and reperfusion. I/R elicited a comparable degree of polymorphonuclear (PMN) infiltration in mucosa, submucosa, and mesentery, with the muscularis exhibiting a greater response. Pretreatment with the CD18-specific monoclonal antibody (IB4) significantly attenuated the I/R-induced PMN accumulation in all layers of the bowel wall and mesentery, indicating that the granulocyte accumulation elicited by I/R is dependent on the expression and/or activation of the leukocyte adhesion molecule CD11/CD18.

Carbohydrase activity in the pancreatic tissue and small intestine mucosa of sheep fed dried-grass or ground maize-based diets

1985 ◽  
Vol 104 (2) ◽  
pp. 435-443 ◽  
Author(s):  
A. N. Janes ◽  
T. E. C. Weekes ◽  
D. G. Armstrong
Keyword(s):  
Small Intestine ◽  
Amylase Activity ◽  
Total Activity ◽  
Pancreatic Tissue ◽  
Proximal Region ◽  
Small Intestinal Mucosa ◽  
Intestine Mucosa ◽  
Ruminant Animals ◽  
Specific Activities ◽  
Small Intestinal

SummaryTwo groups of six sheep were fed either dried-grass or ground maize-based diets for at least 4 weeks before slaughter. Samples of the small intestinal mucosa and spancreatic tissue were assayed for a-amylase, glucoamylase, maltase and oligo-l,6-glucosidase.The pancreatic tissue contained high activities of α-amylase and much lower activities of glucoamylase, maltase and oligo-1,6-glucosidase. There was no effect of diet on the specific activities of any of these enzymes in the pancreatic tissue.The activity of α-amylase adsorbed on to the mucosa of the small intestine was greatest in the proximal region of the small intestine, the activity generally declining with increasing distance away from the pylorus. There was no diet effect on the absorbed α-amylase activity.Similar patterns of distribution along the small intestine were observed for maltase, glucoamylase and oligo-1,6-glucosidase with the highest activities in t he jejunum. There was no overall effect of diet on glucoamylase or maltase specific activities and glucoamylase total activity, although the total activities of maltase and oligo-1,6-glucosidase were significantly greater for the sheep fed the ground maize-based diet (P < 0·05).It is suggested that ruminant animals may be capable of digesting large amounts of starch in the small intestine through an adaptation in the activity of the host carbohydrases.

COX-2/PGE2 Pathway Inhibits the Ferroptosis Induced by Cerebral Ischemia Reperfusion

2022 ◽  
Author(s):  
Yunfei Xu ◽  
Ying Liu ◽  
Kexin Li ◽  
Dun Yuan ◽  
Shun Yang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Cox 2

The nitric oxide donor molsidomine prevents ischemia/reperfusion injury of the adult rat small intestine

2003 ◽  
Vol 19 (4) ◽  
pp. 305-308 ◽  
Author(s):  
Hayrettin Öztürk ◽  
Mustafa Aldemir ◽  
Ali İhsan Dokucu ◽  
Yusuf Yağmur ◽  
Nihal Kilinç ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Rat Small Intestine ◽  
Adult Rat

scholarly journals Protective Effect of Sodium Nitroprusside on the Rat Small Intestine Transplanted Mucosa

2015 ◽  
Vol 2015 ◽  
pp. 1-6
Author(s):  
Feng-Hua Chen ◽  
Ke Li ◽  
Lu Yin ◽  
Chun-Qiu Chen ◽  
Zhao-Wen Yan ◽  
...  
Keyword(s):  
Small Intestine ◽  
Molecular Markers ◽  
Protective Effect ◽  
Sodium Nitroprusside ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Small Bowel Transplantation ◽  
Mucosal Barrier ◽  
No Donor

The intestinal mucosal epithelium is extremely susceptible to even brief periods of ischemia. Mucosal barrier damage, which is associated with ischemia/reperfusion (I/R) injury and consequently bacterial translocation, remains a major obstacle for clinically successful small bowel transplantation (SBT). Previous studies have demonstrated a protective effect of nitric oxide (NO) on other transplanted organs and NO mediated intestinal protection has also been reportedin vitro. The aim of this study was to evaluate the effect of sodium nitroprusside (SNP), NO donor, on graft mucosal histology and molecular markers of function after SBT in rats. We used SNP in different period of heterotopic SBT rats. The groups consisted of SBT, pre-SNP group, and post-SNP group. Interestingly, the pre-SNP graft samples exhibited less damage compared to the SBT and post-SNP samples. In addition, mucosal samples from the pre-SNP group showed higher Na+-K+-ATPase activity and higher levels of laminin expression compared to the SBT and post-SNP samples. The findings of the present study reveal that SNP given before graft ischemia/reperfusion injury has a protective effect on mucosal histology and molecular markers of function in the transplanted small intestine.

scholarly journals Local anesthetic Ropivacaine protects rats from myocardial ischemia/reperfusion injury by inhibition of COX-2

2021 ◽  
Author(s):  
Zhou Yu ◽  
Sufang Sun ◽  
Fang Hu
Keyword(s):  
Oxidative Stress ◽  
Creatine Kinase ◽  
Ischemia Reperfusion ◽  
Inos Expression ◽  
Ischaemic Injury ◽  
Cardiac Tissues ◽  
Tnf Α ◽  
Creatine Kinase Mb ◽  
Cellular Apoptosis ◽  
Cox 2

IntroductionMyocardial ischaemia/reperfusion (I/R) injury is the leading cause of morbidity and mortality worldwide. Despite novel advances in therapeutics, the management of myocardial I/R is still an unmet medical need. Therefore, in the present study, we have demonstrated the protective effect of ropivacaine (RPC) on the myocardial infarction in rats and its underlying mechanism.Material and methodsInitially, the effect of RPC was determined on the infarct size and histopathology of cardiac tissues. The effect of RPC was also determined on the levels of various cardiac biomarkers such as creatine kinase (CK), creatine kinase MB (CK-MB), alanine aminotransferase (ALT), asparganine aminotransferase (AST), and lactate dehydrogenase (LDH), and biomarkers of oxidative stress (MDA, SOD, and GSH) and inflammation (tumour necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and IL-6). RPC effect was also quantified on cellular apoptosis and COX-2 and iNOS expression via western blot analysis. The RPC was further docked into the active site of COX-2.ResultsIt has been found that RPC reduces the improves haemodynamics of (LVSP and ± dp/dtmax, and LVEDP), infarct percentage and architecture of cardiac tissues of rats. It also reduces the level of studies cardiac injury biomarkers together with a reduction of oxidative stress (MDA, SOD, and GSH) and inflammation (TNF-α, IL-1β, and IL-6). Upon administration of RPC, the rate of cellular apoptosis was found to be greatly reduced, with a reduction in COX-2 and iNOS expression. In docking analysis, RPC creates van der Waals forces and pi-interactions with Tyr381, Arg106, Val102, Leu345, Val509, Ser339, Leu338, Val335, Ala513, His75, and Leu517 at the catalytic site of COX-2.ConclusionsCollectively, our results demonstrated that ropivacaine showed significant benefit against myocardial ischaemic injury.

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