Abstract

The aim of the present study was to investigate the protective effect of crocin on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rats. Thirty-two male rats were randomly divided into sham, I/R, I/R + crocin pretreatment and crocin alone groups. To induce I/R lesions, the celiac artery was clamped for 30 min, and the clamp was then removed to allow reperfusion for 3 h. Crocin-pretreated rats received crocin (15 mg/kg, i.p.) 30 min prior to the induction of I/R injury. Samples of gastric mucosa were collected to quantify the protein expression of caspase-3, an apoptotic factor, and inducible nitric oxide synthase (iNOS), a pro-inflammatory protein, by Western blot. Pretreatment with crocin decreased the total area of gastric lesions and decreased the protein expression levels of caspase-3 and iNOS induced by I/R injury. Our findings showed a protective effect of crocin in gastric mucosa against I/R injury. This effect of crocin was mainly mediated by reducing the protein expression of iNOS and caspase-3.

Highlights

  • It is well established that reactive oxygen species (ROS) and reactive nitrogen species (RNS) are involved in the development of gastric ischemia-reperfusion (I/R) injury (Yoshikawa et al, 1989, Ishii et al, 2000)

  • The results of this study showed that: (1) pretreatment with crocin decreased the total surface area of the acute gastric mucosal lesions induced by I/R; (2) the protein expression level of inducible nitric oxide synthase (iNOS) was lower in crocin-pretreated rats than in the I/R injury rats; and (3) the protein expression level of active caspase-3 was higher in the I/R injury rats than in I/R+crocin-pretreated and sham-operated rats

  • The present results showed that pretreatment with crocin significantly reduced mucosal lesions and the level of iNOS expression

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Summary

Introduction

It is well established that reactive oxygen species (ROS) and reactive nitrogen species (RNS) are involved in the development of gastric ischemia-reperfusion (I/R) injury (Yoshikawa et al, 1989, Ishii et al, 2000). Mansouri modification and leading to cellular injury (Huang et al, 2011, Yang et al, 2012)

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