S-Aspirin Protects Aspirin-Induced Gastric Injury Figure 5. Effect of ACS14 on levels of MDA (A) and GSH (B) and protein expressions of SOD1 (C) and XOD (D) of gastric tissues in Asp-treated rats. Data are presented as means6SE. n = 4–8. *P,0.05 compared with control; #P,0.05 compared with Asp; {P,0.05 compared with Asp+ACS14 1 mg/kg. doi:10.1371/journal.pone.0046301.g005 NaHS, which didn’t influence the protective role on Asp-induced gastric injury. This is consistent with the previous findings that NaHS can inhibit NADPH oxidase expression and concomitant O2.2 formation [25,57–59]. XOD catalyzes the conversion reactions of hypoxanthine to xanthine and xanthine to uric acid, the last reaction in the purine catabolism, with byproduct of toxic superoxide radical. In this regard, it is a key enzyme between purine and free radical metabolism [60]. It was reported that XOD is an endogenous source of ROS and reactive nitrogen species (RNS) that can induce oxidative stress and inflect tissue injury [61]. Our findings showed that Asp significant increased XOD protein level in gastric tissue and this effect was reversed by ACS14. Taken together, our data clearly demonstrated that ACS14 may protect gastric mucosa by suppression of oxidative stress. We also investigated the effect of ACS14 on the gastric blood flow. It was found that ACS14 obviously increased Asp-reduced gastric blood flow. This may further contribute to its anti-oxidant effect as sufficient blood flow and oxygen supply may wash-out/ inhibit Asp-induced O2.2 production in gastric tissue. The PLOS ONE | www.plosone.org 7 September 2012 | Volume 7 | Issue 9 | e46301