Aim. To investigate the effect of Ginsenoside Rb1 (GS-Rb1) on hypoxia/ischemia (H/I) injury in cardiomyocytes in vitro and the\nmitochondrial apoptotic pathway mediated mechanism. Methods. Neonatal rat cardiomyocytes (NRCMs) for the H/I groups were\nkept in DMEMwithout glucose and serum, and were placed into a hypoxic jar for 24 h. GS-Rb1 at concentrations from2.5 to 40 ????M\nwas given during hypoxic period for 24 h. NRCMs injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay.\nCell apoptosis, ROS accumulation, and mitochondrial membrane potential (MMP) were assessed by flow cytometry. Cytosolic\ntranslocation of mitochondrial cytochrome c and Bcl-2 family proteins were determined byWestern blot. Caspase-3 and caspase-9\nactivities were determined by the assay kit. Results. GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I. It\nalso reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst.\nMoreover,GS-Rb1markedly decreased the translocation of cytochrome c from themitochondria to the cytosol, increased the Bcl-2/\nBax ratio, and preserved mitochondrial transmembrane potential (??m). Its administration also inhibited activities of caspase-9\nand caspase-3. Conclusion. Administration of GS-Rb1 during H/I in vitro is involved in cardioprotection by inhibiting apoptosis,\nwhich may be due to inhibition of the mitochondrial apoptotic pathway
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