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
Summary
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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