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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2005, Vol. 10 ›› Issue (9): 1010-1014.

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Protective effects of preconditioning of Ginsenoside Rb1 on neonatal rat cardiomyocytes against hypoxia-reoxygenation injury

GUO Jia, LIU Xiao-kang, WU Wen, ZHANG Xiao-wen1   

  1. Department of Pharmacology, West China School of Basic Medical Science and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan, China;
    1Department of Basic Theory of Traditional Chinese Medicine, Basic Medicine College of Guangzhou University of Traditional Chinese Medicine, Guangzhou 510405, Guangdong, China
  • Received:2005-01-20 Revised:2005-04-26 Published:2020-11-22

Abstract: AIM: To study the effects and mechanisms of preconditioning of Ginsenoside Rb1 (Rb1) on neonatal rat cardiomyocytes against hypoxia-reoxygenation (H/R) injury.METHODS: Myocytes hypertrophy model was induced by Angiotensin II in neonatal rat and determined by assaying the cell surface area(CSA) and total protein content (TP) of cardiomyocytes.The H/R model was established after treatment with Rb1 for 48 h.The cell survival ability was assayed by MTT method.The apoptotic rate was assayed by flow cytometry.The activities of lactate dehydrogenase (LDH), content of nitric oxide (NO) and malondialdehyde (MDA) in medium were measured.RESULTS: After treatment of cells with Rb1 (0.01-10.00 μmol·L-1) for 48 h, compared with the H/R group, the myocyte CSA reduced by 41.56%, the TP lowered by 43.37%.The LDH activity reduced by 59.20%, the content of MDA decreased by 72.03%, the apoptosis rate reduced by 85.29%, the cell survival increased by 2.28 fold and NO activity enhanced by 2.67 fold (P <0.01).CONCLUSION: Ginsenoside Rb1 preconditioning can protect AngII-induced hypertrophy myocardium against H/R injury, increase myocyte viability and decrease total protein content.And these effects are related to reducing apoptosis and the release of LDH, improving activities of NO and decreasing the level of lipid peroxidation.

Key words: Ginsenoside Rb1, hypoxia-reoxygenation, hypertrophy, cardiomyocytes, LDH, apoptosis, nitric oxide, MDA

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