The results showed that gallic acid significantly decreased the protein expression of caspase-3. injury, Rat == Intro == It is well established that reactive oxygen species (ROS) and reactive nitrite species (RNS) are involved in development of gastric ischemia-reperfusion injury. 1, 2Also, contribution of nitric oxide (NO) in I/R-induced gastric lesions continues to be documented. 3It has been shown that NO reacts with ROS and produces highly toxic substances such as peroxynitrite and singlet oxygen. 4, 5Naturally, NO is produced from L-arginine in mammalian tissues by three isoforms of NO synthase, two constitutive (eNOS and nNOS) and 1 inducible (iNOS) form. In the oxidative stress iNOS gene transcription and promoter activity are increased and it regulates chromatin modification leading to cellular injury. 6, 7 Acute gastric mucosal injury has been reported as a result of decreased blood flow and alterations in gastric microvascularization, 8that leads to ischemia reperfusion injury (I/R). The ischemia followed by reperfusion during gastric I/R injury develops mucosal inflammation which in turn often leads to hemorrhagic types of inflammation. These changes serve as a perquisite intended for mucosal erosions. 9The pathophysiology of I/R-induced injury is associated with inflammatory responses that elicit tissue damage. The acute inflammatory response is Nutlin-3 characterized by induction of inflammatory cytokines, 10neutrophil infiltration, 11and generation of oxygen free radicals. 1, 12 Gallic acidity is also known as 3, 4, 5-trihydroxybenzoic acidity, found in gallnuts, sumac, witch hazel, green tea, oak bark, pineapple, grapes and other plants. 13Gallic acid has been shown to possess strong anti-oxidative activity and many reports have shown that neuro-, cardio-, and hepato-protective effects of gallic acid. 14-17Additionally, gallic acidity has been shown to protect the gastric mucosa against ethanol-, and aspirin-induced gastric lesions in rats. 18, 19The gastric I/R-injury is an important and common clinical problem which could result in mucosal erosions and ulcers. There are some clinical conditions that are contributed to gastric I/R injury-including peptic ulcer bleeding, vascular rupture or surgery, ischemia gastrointestinal disease and hemorrhagic shock. 20However, the satisfactory clinical techniques to treat the gastric I/R injury are rare. 21, 22Therefore, promoting the cells levels of antioxidants by pretreatment therapy can attenuate cells damages following ischemia-reperfusion-induced injury. To the best of our knowledge, there is no report about the effect of gallic acid on gastric mucosa following I/R injury in rat. Therefore , the aim of the present study was to evaluate the protecting effect of gallic acid on gastric mucosal lesions induced by I/R injury in rat by evaluating the changes in the degree of the protein expression of apoptotic element, caspase-3, and pro-inflammatory protein, inducible nitric oxide synthase (iNOS) in gastric mucosa. == Components and methods == Animals. Nutlin-3 Forty male Wistar rats (body weight 150 to 200 g) Ednra were purchased from the creature house of Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. The animals were Nutlin-3 fed on standard diet and had free access to tap water. They were maintained Nutlin-3 under standard conditions of humidity, temperature (22 2 C) and 12 hr light/dark cycle. The animals were deprived of food but not water immediately before intervention. All experiments were carried out in accordance with the regulations arranged by ethics committee of Ahvaz Jundishapur University of Medical Sciences (research project PRC156). Chemicals. Gallic acidity (G7384; Purity: 100 2 . 5%), was purchased from Sigma (St. Louis, USA). Ketamine hydrochloride and xylazine hydrochloride were purchased from Alfasan (Woerden, The Netherlands). Animal grouping and experimental procedures. The rats were randomly assigned to the same five groups (n = 8): Control, gallic acid-treated (15, 30 or 60 mg kg-1, intraperitoneally) and sham groups. Gastric I/R injury was induced according to the method of Wadaet al. 23Briefly, under an intraperitoneal injection of 60 mg kg-1ketamine and 15 mg kg-1xylazine mixture), the rats underwent a midline laparotomy and the celiac artery was carefully isolated from its adjacent tissues. The celiac.