Effect of endogenous hydrogen sulfide on oxidative stress in oleic acid-induced acute lung injury in rats

Background Acute lung injury （ALl） is a common critical disease in emergency care. Oxidative stress plays an important role in the pathogenesis of ALl. Endogenous hydrogen sulfide （H2S） can inhibit oxidative stress in rat gastric mucosal epithelium. In this study, we examined the possible role of H2S in regulation of the oxidative stress in oleic acid-induced acute lung injury in rats. Methods The rat model of ALl was induced by intra-tail vein injection of oleic acid （CA）. NariS solution was injected intraperitoneally before CA injection as an CA＋NariS group. A semi-quantitative histological index of quantitative assessment of lung injury was calculated. The levels of superoxide dismutase （SOD）, glutathione （GSH） and malondialdehyde （MDA） in plasma and lung tissue were detected with ELISA. The levels of H2S content in lung tissue were detected with an ion meter. Results Compared with the control group, the level of H2S in lung tissue was significantly decreased, and the level of SOD and GSH were decreased but the level of MDA was increased in plasma and lung tissue in rats with ALl. NariS lessened the ALl in association with an increase in the level of H2S in lung tissue, a decrease in the level of MDA but an increase in SOD and GSH levels in plasma and lung tissues. Conclusion Endogenous H2S could inhibit the oxidative stress in lung tissue in oleic acid-induced acute lung injury in rats.