Abstract
Objectives: This study aimed to assess the possible antioxidant role of sitagliptin on intestinal ischemia/reperfusion (II/R)-mediated tissue injury. Methods: Forty-five male Sprague-Dawley rats were randomly assigned into three groups: Sham group (operation without clamping), II/R group (operation with clamping) and Sitagliptin pretreated group (300 mg/kg/day; orally by gavage) for 2 weeks before II/R insult. II/R was performed by clamping the superior mesenteric artery for 30 min, followed by 60 min reperfusion after removal of clamping. At the end of the experimental period, all rats were sacrificed for biochemical assessment of oxidative stress parameters. Results: Pretreatment with sitagliptin remarkably alleviated the oxidative stress response induced by I/R in the jejunum manifested by a marked reduction of the pro-oxidant NOX-2 enzyme level, the lipid peroxidation marker, MDA content and the nitrosative stress indicator, NO content as well as replenishing the key cellular enzymatic antioxidant, SOD activity. Conclusion: Sitagliptin has a potential antioxidant effect against II/R injury in rats and thus we assume sitagliptin may be a beneficial prophylactic drug in patients at risk of intestinal I/R injury.
Highlights
Ischemia/reperfusion (I/R) injury occurs when tissues or organs are subjected to a period of ischemia, followed by blood flow replenishment
Effect of sitagliptin on the intestinal nicotinamide adenine dinucleotide phosphate oxidase (NOX)-2 enzyme level in rats subjected to II/R injury
I/R induced a marked increase in intestinal nicotinamide adenine dinucleotide phosphate oxidase-2 (NOX-2) enzyme level by 181% compared to the Sham group
Summary
Ischemia/reperfusion (I/R) injury occurs when tissues or organs are subjected to a period of ischemia, followed by blood flow replenishment. Intestinal ischemia/reperfusion (II/R) injury is inevitable under numerous clinical conditions, such as in mesenteric artery embolism, intestinal transplantation, cardiopulmonary bypass, abdominal aortic aneurysm surgery, and traumatic or hemorrhagic shock[1]. Induction of ischemia and reperfusion to the small intestine, compared to other organs, is ferocious as damage to the mucosal barrier integrity results in bacterial translocation, eventually leads to multiple organ failure, and death[2]. It has been demonstrated that reactivation of aerobic metabolism to the small intestine by reperfusion after an adequate period of ischemia, is associated with a burst production of reactive oxygen and nitrogen species (ROS/RNS) such as superoxide anion, hydrogen http://aprh.journals.ekb.eg/ 234
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