CARVACROL REDUCES THE SEVERITY OF INTESTINAL MUCOSAL DAMAGE CAUSED BY INTESTINAL ISCHEMIA – REPERFUSION IN RATS

Abstract

Intestinal ischemia-reperfusion (I/R) is a pathophysiological process that is common in many clinical conditions such as shock, sepsis, mesenteric thrombosis, necrotizing enterocolitis, and bowel transplantation. Our aim in this study was to investigate the potential protective effects of carvacrol on the intestinal I/R injury in a rat model. The 30 rats were randomly divided into three groups (n = 10): The sham-control (group 1) underwent only the separation of the superior mesenteric artery but not the occlusion. In the I/R-untreated (group 2) and I/R-carvacrol-treated groups (group 3), the superior mesenteric artery was clamped for 45 min, followed by 60 min of reperfusion. 2 hours before ischemia, the group 3 of rats received an intraperitoneal injection of carvacrol at a dose of 75 mg/kg bw. At the end of the experiment, intestinal tissue samples were taken for oxidative stress assessment including superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO), total antioxidant status (TAS) and total oxidant status (TOS). In addition, the intestine sections were stained with haematoxylin-eosin to evaluate morphological changes and immunohistochemical staining was performed for inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) assessment. The intestinal mucosa was significantly damaged in the group 2, which was markedly attenuated after carvacrol treatment. The tissue MDA, MPO and TOS content increased significantly in the group 2, but they were reduced by carvacrol treatment. In addition, SOD and TAS activity increased markedly in group 3 as compared to group 2. Immunohistochemical staining showed that iNOS increased and eNOS decreased in group 2, which was improved in reverse direction after carvacrol treatment. Carvacrol may be a potential therapeutic agent for the treatment of intestinal I/R injury.