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Abstract

Objectives: The purpose of this study was to evaluate the effect of intravenous injection of osthole on intestinal ischemia-reperfusion injury and parameters of oxidative stress. Materials and Methods: In 45 Kunming male mice, treatment included sham surgery (15 mice); intestinal ischemia-reperfusion injury (clamping of the superior mesenteric artery, 2 h; clamp release, 1 h; 15 mice); or osthole treatment before and after ischemia-reperfusion injury (15 mice). Evaluation included histopathology, determination of intestinal wet/dry weight ratio, and measurement of levels of diamine oxidase, superoxide dismutase, malondialdehyde, interleukin 1β, tumor necrosis factor α, and interleukin 2. Intestinal barrier permeability was evaluated with Evans blue test. Results: The mean wet-to-dry weight ratio, Evans blue content, and Chiu score were significantly greater in the ischemia-reperfusion than in the sham group and lower in the osthole-treated than the ischemia-reperfusion group. The mean serum diamine oxidase, malondialdehyde, interleukin 1β, and tumor necrosis factor α levels were significantly greater in the ischemia-reperfusion than in the sham group and lower in the osthole-treated than in the ischemia-reperfusion group. The mean superoxide dismutase activity and interleukin 2 levels were lower in the ischemia-reperfusion than in the sham group and greater in the osthole-treated than in the ischemia-reperfusion group. Conclusions: Treatment with osthole may protect against oxidative stress and tissue damage from intestinal ischemia-reperfusion injury.

Inhibition of Prolyl Oligopeptidase Prevents Consequences of Reperfusion following Intestinal Ischemia

“…Mesenteric ischemia (MI) is a severe pathological event associated with a varied number of diseases such as vessel obstruction, hernias, and septic shock often resulting in morbidity and death [1]. MI essentially leads to developing acute and chronic inflammatory conditions of the intestine and in the worst case developing intestinal ischemia (II) [2]. The II refers to a complex consequence including loss of organ-specific activity, alteration of gut microbiota, tissue necrosis, and the release of proinflammatory cytokines (interleukin 1β [IL-1β] and tumor necrosis factor α [TNF-α]) and reactive oxygen species (ROS).…”