Physiology Research Center (PRC), Research institute for infectious diseases of digestive system and Dept. of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
The present study aimed to evaluate the protective effect of crocin on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rats.Forty male rats were randomly divided into sham, control (I/R injury) and three crocin-pretreated groups. To induce I/R lesions, the celiac artery was clamped for 30 min and then the clamp was removed to allow reperfusion for 3 h. Pretreated-rats received crocin (7.5, 15 or 30 mg/kg, i.p.) 30 min prior to the induction of I/R injury. Samples of gastric mucosa were collected to measure the following variables: 1. mRNA expression of superoxide dismutase (SOD) and glutathione peroxidase (Gpx) by RT-PCR; 2.activity of superoxide dismutase and glutathione peroxidase and 3.tissue levels of malonyldehaldehyde (MDA). Pretreatment with crocin decreased the total area of gastric lesions. Messenger RNA expressions of SOD and Gpx in control I/R injury rats were significantly decreased as compared with sham-operated group (P<0.001). Crocin pretreatment 30 min prior to I/R injury significantly increased mRNA expressions of SOD and Gpx genes. The gastric mucosal activities of SOD and Gpx in control I/R injury rats were significantly lower than in crocin-pretreated groups (P<0.01). Crocin pretreatment decreased mucosal production of MDA. Our findings showed the protective effect of crocin on gastric mucosa against ischemia-reperfusion injury. These effects of crocin were mainly mediated by increasing the mRNA expressions- and the enzyme activity of SOD and Gpx as well as by inhibiting the production of free radicals.