Seyyed Ali Mard - Physiology Research Center (PRC), Research Center for Infectious Diseases of Digestive System, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Shahnaz Mojadami - Physiology Research Center (PRC), Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Yaghoob Farbood - Physiology Research Center (PRC), Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Mohammad Kazem Gharib Naseri - Physiology Research Center (PRC), Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

The present study aimed to evaluate the protective effect of gallic acid on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rat. Forty male rats were randomly divided into sham, control (I/R injury) and three gallic acid-pretreated groups. To induce I/R lesions, the celiac artery was clamped for ۳۰ min and then the clamp was removed to allow reperfusion for ۶ hr. Pretreated rats received gallic acid (۱۵, ۳۰ or ۶۰ mg kg-۱, intraperitoneally) ۳۰ min prior to the induction of I/R injury. Macroscopic and microscopic evaluations of the areas of ulceration were compared. Samples of gastric mucosa were collected to evaluate the protein expression of pro-apoptotic factor, caspase-۳, and pro-inflammatory enzyme, inducible nitric oxide synthase (iNOS) using western blot. Pretreatment with gallic acid decreased the total area of gastric lesions. Gallic acid at ۳۰ mg kg-۱ decreased the levels of protein expression of caspase-۳ and iNOS induced by I/R injury. Our findings showed the protective effect of gallic acid on gastric mucosa against ischemia-reperfusion injury. This effect of gallic acid was mainly mediated by reducing protein expression of iNOS and caspase-۳.

Caspase-۳, Gallic acid, Inducible nitric oxide synthase, Ischemia-reperfusion injury, Rat