Protective effect of endogenous hydrogen sulfide against oxidative stress in gastric ischemia-reperfusion injury

Hydrogen sulfide (H2S) is a gaseous signaling molecule, which plays a critical role in a number of physiological and pathological progresses. In order to determine the effect of endogenous H2S on gastric ischemia-reperfusion (GI-R), we evaluated the gastric mucosal damage in rats intraperitoneally injected with DL-propargylglycine (PAG, 50 mg/kg/day) or L-cysteine (L-cys, 50 mg/kg/day) for 7 days before GI-R. GI-R injury was achieved by clamping the celiac artery for 30 min, followed by reperfusion for 60 min. Gastric mucosal damage was macroscopically assessed in the area of injury and deep damage was assessed by histopathological scoring. PAG increased the area of gastric mucosal injury and deep damage compared with that in untreated GI-R rats (P<0.05). While PAG decreased the H2S concentration and cystathionine gamma-lyase (CSE) expression in the gastric mucosa, L-cys significantly attenuated the effects of GI-R. Western blot analysis revealed that the increases of malondialdehyde (MDA) and xanthine oxidase (XOD), and decreases of glutathione (GSH), superoxide dismutase (SOD) and the restriction of superoxide (O-2(-)) production in the PAG group were inhibited by L-cys (P<0.05). Endogenous H2S has a protective effect against GI-R in rats by inhibiting oxygen free radical overproduction.