Melatonin reduces bacterial translocation after intestinal ischemia-reperfusion injury

Melatonin, the primary pineal hormone, has been reported to protect from oxidative injury after ischemia-reperfusion (IR). The aim of this study was to evaluate the effects of exogenous melatonin on intestinal integrity, ileal colonization, and bacterial translocation 45-minute after mesenteric IR. Sixteen male ACI rats randomly divided into two groups underwent 45-minutes intestinal ischemia by clamping the superior mesenteric artery. One hour prior to ischemia, study animals (n = 8, group A) were treated with melatonin (10 mg/kg IP) while control animals (n = 8, group B) received the same volume of saline solution. An additional six animals underwent laparotomy and served as a sham-operated group. Animals were sacrificed 24 hours after reperfusion; peritoneal swabs and biopsies of liver, spleen, lung, mesenteric lymph nodes, cecum, and terminal ileum were obtained for microbiology. The ileum samples were also processed for histopathological evaluation of IR-induced injury. Twenty-four hours after reperfusion bacterial translocation to the peritoneal cavity present in all group B animals was reduced to 37.5% among those that were melatonin-treated (group A; P < .05). Furthermore bacterial translocation to mesenteric lymph nodes, spleen, and liver was significantly lower in group A than group B (P < .05). Although cecal and ileal counts did not differ between the two groups, ileal counts from control animals showed increased colonization. Accordingly, a single injection of exogenous melatonin significantly reduced the intestinal IR injury and prevented bacterial translocation.