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Evidence-Based Complementary and Alternative Medicine
Volume 2014 (2014), Article ID 149195, 10 pages
Research Article

Ginsenoside Rb1 Protects Neonatal Rat Cardiomyocytes from Hypoxia/Ischemia Induced Apoptosis and Inhibits Activation of the Mitochondrial Apoptotic Pathway

1Beijing Haidian Hospital (Haidian Section of Peking University Third Hospital), 29 Zhongguancun Dajie, Haidian District, Beijing 100080, China
2Postdoctoral Workstation of the Zhongguancun Haidian Science Park, NO. 6, Sijiqing Road, Haidian District, Beijing 100195, China
3Institute of Geriatric Cardiology, The General Hospital of People’s Liberation Army, 28 Fuxing Road, Beijing 100853, China
4Beijing Hospital of Integrated Traditional Chinese and Western Medicine, Dongjie 3, Yongding Road, Haidian District, Beijing 100039, China
5Beijing Institute of Radiation Medicine, Beijing 100850, China

Received 1 April 2014; Revised 2 June 2014; Accepted 23 June 2014; Published 10 July 2014

Academic Editor: Ke-Ji Chen

Copyright © 2014 Xu Yan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aim. To investigate the effect of Ginsenoside Rb1 (GS-Rb1) on hypoxia/ischemia (H/I) injury in cardiomyocytes in vitro and the mitochondrial apoptotic pathway mediated mechanism. Methods. Neonatal rat cardiomyocytes (NRCMs) for the H/I groups were kept in DMEM without glucose and serum, and were placed into a hypoxic jar for 24 h. GS-Rb1 at concentrations from 2.5 to 40 µM was given during hypoxic period for 24 h. NRCMs injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. Cell apoptosis, ROS accumulation, and mitochondrial membrane potential (MMP) were assessed by flow cytometry. Cytosolic translocation of mitochondrial cytochrome c and Bcl-2 family proteins were determined by Western blot. Caspase-3 and caspase-9 activities were determined by the assay kit. Results. GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I. It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst. Moreover, GS-Rb1 markedly decreased the translocation of cytochrome c from the mitochondria to the cytosol, increased the Bcl-2/ Bax ratio, and preserved mitochondrial transmembrane potential (ΔΨm). Its administration also inhibited activities of caspase-9 and caspase-3. Conclusion. Administration of GS-Rb1 during H/I in vitro is involved in cardioprotection by inhibiting apoptosis, which may be due to inhibition of the mitochondrial apoptotic pathway.