Sulfur dioxide preconditioning increases antioxidative capacity in rat with myocardial ischemia reperfusion (I/R) injury

• SO2 preconditioning reduced I/R-induced myocardial injury.
• SO2 preconditioning upregulated myocardial H2S/CSE pathway.
• SO2 preconditioning downregulated NO/iNOS pathway.
• SO2 preconditioning significantly increased myocardial antioxidative capacity.

BackgroundThe study was designed to explore if sulfur dioxide (SO2) preconditioning increased antioxidative capacity in rat with myocardial ischemia reperfusion (I/R) injury.MethodsThe myocardial I/R model was made by left coronary artery ligation for 30 min and reperfusion for 120 min in rats. Myocardial infarct size and plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activities, plasma superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and glutathione (GSH) changes were detected for the rats. The contents of myocardial hydrogen sulfide (H2S) and nitric oxide (NO) were measured. Myocardial protein expressions of SOD1, SOD2, cystathionine γ-lyase (CSE) and iNOS were tested using Western blot.ResultsMyocardial infarction developed and plasma CK and LDH activities were significantly increased in I/R group compared with those in control group, but SO2 preconditioning significantly reduced myocardial infarct size, and plasma CK and LDH activities. SO2 preconditioning successfully increased plasma SOD, GSH and GSH-Px levels and myocardial SOD1 protein expression, but decreased MDA level in rats of I/R group. Compared with controls, the myocardial H2S level and CSE expression were decreased after I/R, but myocardial NO level and iNOS expression were increased. With the treatment of SO2, myocardial H2S level and CSE expression were increased, but myocardial NO level and iNOS expression were decreased compared with those in I/R group.ConclusionsSO2 preconditioning could significantly reduce I/R-induced myocardial injury in vivo in association with increased myocardial antioxidative capacity, upregulated myocardial H2S/CSE pathway but downregulated NO/iNOS pathway.