Ry induced by Z-DEVD-FMK site absolute ethanol. In quantitative analysis, BCT reduced the elevated gastric injury index induced by absolute ethanol treatment. NC, normal control; EtOH, absolute ethanol treatment group; Ome, absolute ethanol + omeprazole (50 mg/kg); BCT, absolute ethanol + BCT (400 mg/kg). ##Significantly different at p < 0.01 compared with the control group, *Significantly different at p < 0.05 compared with the EtOH group.the MDA levels, and increased the levels of antioxidants including GSH, catalase, GST, GPx, GR, and SOD. An acute gastric injury model induced by factors that play a role in gastric disorder etiopathogenesis was used to investigate the protective effects of novel materials [22,23]. It is known that stress, alcohol, and steroidal/ nonsteroidal inflammatory drugs are some of the factors that increase gastric injury including hemorrhage, erosion, and ulceration [24]. The roles of ROS in the pathogenesis of ethanol induced gastric injury have been demonstrated. ROS cause tissue damage and their levels are reduced byantioxidant defense systems including GSH, catalase, GPx, GR, SOD, and GST [25-27]. These defense systems protect the stomach tissue from the PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28506461 increased ROS production induced by ethanol intake. The gastric injury induced by ethanol intake begins with the formation of lipid radicals in the cell membranes, which damages and destroys the cell membranes [25]. GSH is an endogenous antioxidant component and its activity is related to the thiol group of cysteine in its structure [24]. GSH reacts with peroxides and toxic oxygen radicals such as the hydroxyl ion and singlet oxygen to protect cells from injury [28]. InShin et al. BMC Complementary and Alternative Medicine 2013, 13:170 http://www.biomedcentral.com/1472-6882/13/Page 6 ofFigure 3 Histopathology of the gastric mucosa. Absolute ethanol induced hemorrhagic and the loss of gastric epithelial cells (magnification: ?00). By contrast, BCT attenuated the gastric mucosal injuries induced by absolute ethanol.this study, administration of BCT exhibited a singfincant reduction in the MDA level, a lipid peroxidation product compared with the animals given ethanol (EtOH group). In contrast, the GSH levels were significantly decreased in the EtOH group compared with the normal control, whereas the BCT treated group had higher GSH levels than the EtOH group. These differences are compatible with previous studies [21,27,29]. The levels of enzymatic antioxidant defense components such as catalase, GST, GPx, GR, and SOD were decreased by ethanol intake. By contrast, administration of BCT increased the activities of antioxidant enzymes compared with the EtOH group. SOD is an important antioxidant enzyme that converts superoxide to hydrogen peroxide and oxygen [30]. Thus, it protects aginst the oxidative stress induced in cells and tissues by various stimuli. Inaddition, catalase catalyzes the decomposition of hydrogen peroxide to water and oxygen, which protects aginst damage to cells and tissues [31]. GST catalyzes the conjugation of GSH via a sulfhydryl group to the electrophilic centers of a wide variety of substrates [24]. These processes detoxify endogenous toxic materials such as peroxidized lipids. GPx is an enzyme with peroxidase activity, which reduces lipid hydroperoxides and free hydrogen peroxide to water [26]. GR is an important antioxidant enzyme that reduces glutathione disulfide to the sulfhydryl form of GSH [32]. Many previous studies have demonstrated that e.