2,3,5,4′-Tetrahydroxystilbene-2-O-β-d-glucoside eliminates ischemia/reperfusion injury-induced H9c2 cardiomyocytes apoptosis involving in Bcl-2, Bax, caspase-3, and Akt activation

ObjectiveThis study was designed to explore the protective effect of 2,3,5,4-tetrahydroxystilbene-2-O--d-glucoside (TSG) against ischemia/reperfusion (I/R) injury-induced cardiomyocytes apoptosis. MethodsThe H9c2 cell I/R injury model was induced by simultaneous shortage of nutrients and oxygen. TSG administration (0.10, 0.25, and 0.50mM) was performed before and during I/R stimulation. Cell apoptosis was evaluated using terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Expression of cell-related proteins was detected to assess the effect of TSG on cell apoptosis. ResultsI/R injury induced significant cell apoptosis. Significantly decreased Bcl-2 and increased Bax, caspase-3, and p-Akt expression (P<0.01) was detected in the cell model of I/R injury. In contrast, TSG administration eliminated all the changes induced by I/R injury in a dose-dependent manner. Compared with the H9c2 cell model of I/R injury, the H9c2 cells treated with 0.50mM TSG showed the lowest cell apoptosis percentage, the highest expression of Bcl-2, and the lowest expression of Bax, caspase-3, and p-Akt (P<0.01). ConclusionWe confirmed that the protective effect of TSG against I/R injury-induced cell apoptosis in H9c2 in vitro was associated with the Bcl-2/Bax ratio, caspase-3, and Akt activation.