AICAR attenuates inflammatory response and tissue injury after intestinal ischemia-reperfusion

Objectives. Intestinal ischemia-reperfusion injury is associated with mucosal damage and has a high rate of mortality. Various beneficial effects of ozone have been shown. The aim of the present study was to show the effects of ozone in ischemia reperfusion model in intestine.Material and Method. Twenty eight Wistar rats were randomized into four groups with seven rats in each group. Control group was administered serum physiologic (SF) intraperitoneally (ip) for five days. Ozone group was administered 1 mg/kg ozone ip for five days. Ischemia Reperfusion (IR) group underwent superior mesenteric artery occlusion for one hour and then reperfusion for two hours. Ozone + IR group was administered 1 mg/kg ozone ip for five days and at sixth day IR model was applied. Rats were anesthetized with ketamine∖xyzlazine and their intracardiac blood was drawn completely and they were sacrificed. Intestinal tissue samples were examined under light microscope. Levels of superoxide dismutase (SOD), catalase (CAT), glutathioneperoxidase (GSH-Px), malondyaldehide (MDA), and protein carbonyl (PCO) were analyzed in tissue samples. Total oxidant status (TOS), and total antioxidant capacity (TAC) were analyzed in blood samples. Data were evaluated statistically by Kruskal Wallis test.Results. In the ozone administered group, degree of intestinal injury was not different from the control group. IR caused an increase in intestinal injury score. The intestinal epithelium maintained its integrity and decrease in intestinal injury score was detected in Ozone + IR group. SOD, GSH-Px, and CAT values were high in ozone group and low in IR. TOS parameter was highest in the IR group and the TAC parameter was highest in the ozone group and lowest in the IR group.Conclusion. In the present study, IR model caused an increase in intestinal injury.In the present study, ozone administration had an effect improving IR associated tissue injury. In the present study, ozone therapy prevented intestine from ischemia reperfusion injury. It is thought that the therapeutic effect of ozone is associated with increase in antioxidant enzymes and protection of cells from oxidation and inflammation.

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Intestinal preconditioning prevents systemic inflammatory response in hemorrhagic shock. Role of HO-1

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00348.2001 ◽

2002 ◽

Vol 283 (2) ◽

pp. G408-G414 ◽

Cited By ~ 57

Author(s):

Fabienne Tamion ◽

Vincent Richard ◽

Yann Lacoume ◽

Christian Thuillez

Keyword(s):

Inflammatory Response ◽

Hemorrhagic Shock ◽

Intestinal Ischemia ◽

Ischemia Reperfusion ◽

Systemic Inflammatory Response ◽

Organ Injury ◽

Lung Edema ◽

Heme Oxygenase 1 ◽

Intestinal Ischemia Reperfusion

Intestinal ischemia-reperfusion has been implicated in the systemic inflammatory response and organ injury in hemorrhagic shock, but the exact role of the intestine has never been directly demonstrated. Preconditioning (PC) with brief periods of intermittent ischemia is a known potent anti-ischemic intervention and thus can be used as a tool to assess the role of local intestinal ischemia-reperfusion injury in systemic inflammatory response. Thus rats were first subjected to sham surgery or intestinal preconditioning with four cycles of 1-min ischemia and 10 min of reperfusion 24 h before hemorrhagic shock followed by resuscitation. PC reduced fluid requirements, lung edema, and lactate and tumor necrosis factor-α production. These effects were abolished by the heme-oxygenase-1 (HO-1) inhibitor tin protoporphyrin (Sn-PP). PC induced more than fivefold in intestinal HO-1 expression. These results suggest that intestinal ischemia-reperfusion is a major trigger for inflammatory response and organ injury in nonseptic shock. HO-1 appears to play an important role in the protective effect of intestinal preconditioning.

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Oncostatin M Modulates the Inflammatory Response in Intestinal Ischemia Reperfusion Injury

Journal of Surgical Research ◽

10.1016/j.jss.2013.11.291 ◽

2014 ◽

Vol 186 (2) ◽

pp. 510

Author(s):

P.Y. Young ◽

T.F. Mueller ◽

V.A. Luyckx ◽

C.A. Compston ◽

T.A. Churchill ◽

...

Keyword(s):

Inflammatory Response ◽

Reperfusion Injury ◽

Intestinal Ischemia ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Oncostatin M ◽

Intestinal Ischemia Reperfusion

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Investigating Closed Room Conspirators of Posttraumatic Inflammatory Response: Multi- Omics Profiles of Exosomes Derived from Intestinal Epithelial Cells Under Ischemia Reperfusion Injury

10.21203/rs.3.rs-792334/v1 ◽

2021 ◽

Author(s):

Atsushi Senda ◽

Mitsuaki Kojima ◽

Arisa Watanabe ◽

Tetsuyuki Kobayashi ◽

Keita Nakatsutsumi ◽

...

Keyword(s):

Epithelial Cells ◽

Inflammatory Response ◽

Reperfusion Injury ◽

Intestinal Ischemia ◽

Ischemia Reperfusion Injury ◽

Intestinal Epithelial Cells ◽

Ischemia Reperfusion ◽

Multiple Organ ◽

Intestinal Epithelial ◽

Intestinal Ischemia Reperfusion

Abstract Intestinal ischemia-reperfusion injury leads to multiple organ injuries via gut-derived mediators following severe injury. Growing evidence suggests that exosomes secreted from intestinal epithelial cells are heavily involved in the development of systemic inflammation, but a full elucidation of its pathology remains to be completed. To produce an integrated understanding of its pathology, this study aimed to reveal the changes in exosome content after ischemic stimulation. Our result showed (1) the proteins involved in inflammation by catalyzing RNAs were upregulated, (2) hsa-miR-21-5p, hsa-miR-23a-3p, and hsa-miR-30d-5p levels were increased while hsa-miR-124-3p level was decreased, (3) the increase in unsaturated lysophosphatidylcholines levels. These results together with those of previous studies, suggest that lysophosphatidylcholines may activate the NK-κB pathway. The proteins and microRNAs jointly act to disrupt negative feedback, thereby increasing inflammation. Thus, our results clarify part of the mechanism of multi-organ failure after intestinal ischemic recanalization, thereby providing a new target for treatment.

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