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Evidence-Based Complementary and Alternative Medicine
Volume 2015 (2015), Article ID 171306, 6 pages
Research Article

Ginsenoside-Rb1 Protects Hypoxic- and Ischemic-Damaged Cardiomyocytes by Regulating Expression of miRNAs

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
3Beijing Hospital of Integrated Traditional Chinese and Western Medicine, Dongjie 3, Yongding Road, Haidian District, Beijing 100039, China
4Department of Cardiovascular Surgery, Beijing Aortic Disease Center, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China
5Beijing Institute of Radiation Medicine, Beijing 100850, China

Received 9 July 2014; Revised 25 September 2014; Accepted 2 October 2014

Academic Editor: Hao Xu

Copyright © 2015 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.


Ginsenoside (GS-Rb1) is one of the most important active compounds of ginseng, with extensive evidence of its cardioprotective properties. However, the miRNA mediated mechanism of GS-Rb1 on cardiomyocytes remains unclear. Here, the roles of miRNAs in cardioprotective activity of GS-Rb1 were investigated in hypoxic- and ischemic-damaged cardiomyocytes. Neonatal rat cardiomyocytes (NRCMs) were first isolated, cultured, and then incubated with or without GS-Rb1 (2.5–40 μM) in vitro under conditions of hypoxia and ischemia. Cell growth, proliferation, and apoptosis were detected by MTT and flow cytometry. Expressions of various microRNAs were analyzed by real-time PCR. Compared with that of the control group, GS-Rb1 significantly decreased cell death in a dose-dependent manner and expressions of mir-1, mir-29a, and mir-208 obviously increased in the experimental model groups. In contrast, expressions of mir-21 and mir-320 were significantly downregulated and GS-Rb1 could reverse the differences in a certain extent. The miRNAs might be involved in the protective effect of GS-Rb1 on the hypoxia/ischemia injuries in cardiomyocytes. The effect might be based on the upregulation of mir-1, mir-29a, and mir-208 and downregulation of mir-21 and mir-320. This might provide us a new target to explore the novel strategy for ischemic cardioprotection.