The effect of exogenous hydrogen sulfide postconditioning on myocarial apoptosis and expression of Bcl-2 and Bax protein following ischemia and reperfusion in isolated rat hearts

Objective To investigate the effects of hydrogen sulfide postconditioning on myocardial cell apoptosis following ischemia-reperfusion(I/R) and its relationship with the expressions of Bcl-2 and Bax protein in isolated rat hearts.Methods 42 male SD rat hearts were randomly divided into 3 groups(n=14): sham group,I/R group;hydrogen sulfide postconditioning group(N group).Langendorff isolated rat heart perfusion model was established,followed by equilibrium perfusion for 20 min,40 min of pause and subsequent reperfusion for 60 min.The left ventricular diastolic pressure(LVEDP),left ventricular developed pressure(LVDP),the maximum rate of increase or decrease of left ventricular pressure(±dp/dtmax),heart rate(HR),coronary flow(CF) were recorded at 20 min of equilibrium and 60 min of reperfusion,respectively.At the end of perfusion(20 min),the percentage of myocardial infarct area was measured using triphenyltetrazolium chloride(TTC) staining.The myocardial apoptosis was detected by TUNEL assay to calculate apoptotic index(AI).The semi-quantitative expression of Bcl-2 and Bax was determined with Western blot at the end of reperfusion.Results At the end of equilibrium perfusion,there were no statistical differences in baseline hemodyamics between the experimental groups(P0.05).At the end of reperfusion,compared with I/R group,N group improved hemodynamic injury induced by the I/R(P0.05) and significantly increased the expression of Bcl-2,and greatly decreased the expression of Bax(P0.05).Conclusion Exogenous hydrogen sulfide postconditioning effectively protects isolated rat hearts against ischemia-reperfusion injury by modulating Bcl-2 family proteins.