Many clinical conditions such as shock, sepsis, mesenteric thrombosis, necrotizing enterocolitis, and bowel transplantation can cause intestinal ischemia-reperfusion (IR) injury. This study was designed to determine the effects of leptin on intestinal IR injury. Thirty rats were divided into three groups, each containing ten rats: group A (IR group), group B (treatment group), and group C (sham group). After 1 h of intestinal ischemia, the clamp was removed in order to perform reperfusion. In group B, 100 mg/kg leptin was administered subcutaneously 30 min before reperfusion. In groups A and C, 0.1 ml physiologic saline was injected. In group A, serum and tissue nitric oxide (NO) levels were significantly decreased, and malondialdehyde levels were significantly increased compared to sham group (p < 0.05). Histopathologic injury was significantly lower in sham group compared to group A. In group B, serum and tissue malondialdehyde levels were significantly decreased (p < 0.05), but serum and tissue NO levels were significantly increased compared to group A (p < 0.05). Histopathologic injury was significantly lower in group B compared to group A (p < 0.05). The results of the present study demonstrated that leptin decreases intestinal IR injury by increasing NO production, rearranging mucosal blood flow, and inhibiting polymorphonuclear leukocyte infiltration.
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