Function of PI3/Akt signaling pathway in exogenous hydrogen sulfide postconditioning on isolated rat hearts

Aim To investigate whether the PI3K/Akt signaling pathway participated in hydrogen sulfide postconditioning protecting isolated rat hearts against ischemia/reperfusion injury.Methods 70 male SD rat hearts were isolated and linked to the Langendorff apparatus.They were randomly divided into 5 groups(n=14):ischemia reperfusion group(I/R),hydrogen sulfide postconditioning group(N),DMSO group(D),LY294002 group(L),and hydrogen sulfide with LY294002 group(N+L).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.Myocardial infarct size was measured using triphenyltetrazolium chloride(TTC)staining.Myocardial TUNEL staining was used in situ cell death detection kit.And the percentage of TUNEL positive nuclei to all nuclei counted was used as apoptotic index(AI).The expression of phosphorylation of Akt and total Akt was determined with Western blot analysis at the end of reperfusion.Results There were no differences in baseline hemodyamics observed among the experimental groups(P0.05).After reperfusion,compared with I/R group,N group had better hemodynamics and significantly increased the expression of p-Akt.Meanwhile the myocardial infarct size and cardiocyte apoptotic index were much lower(P0.05).However,LY294002 given during early reperfusion blocked the beneficial effect on hemodyamics,myocardial infarct size and cardiocyte apoptotic index by exogenous H2S postconditioning during reperfusion(P0.05).Meanwhile the expression of p-Akt in L group and N+L group had markedly decreased,compared with N group(P0.05).Conclusion Exogenous hydrogen sulfide postconditioning effectively protects islated rat hearts against ischemia-reperfusion injury by activating PI3K/Akt signaling pathway.