Article Publish Status: FREE
Abstract Title:

Ginsenoside Re Attenuates Isoproterenol-Induced Myocardial Injury in Rats.

Abstract Source:

Evid Based Complement Alternat Med. 2018 ;2018:8637134. Epub 2018 Apr 22. PMID: 29849732

Abstract Author(s):

Quan-Wei Wang, Xiao-Feng Yu, Hua-Li Xu, Yi-Chuan Jiang, Xue-Zhong Zhao, Da-Yuan Sui

Article Affiliation:

Quan-Wei Wang


is widely used for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of. This study aimed to investigate the protective effect of Ginsenoside Re on isoproterenol-induced myocardial injury in rats.Male Wistar rats were orally given Ginsenoside Re (5, 20 mg/kg) daily for 7 days. Isoproterenol was subcutaneously injected into the rats for two consecutive days at a dosage of 20 mg/kg/day (on 6th and 7th day). Six hours after the last isoproterenol injection, troponin T level and creatine kinase-MB (CK-MB) activity were assayed. Histopathologicalexamination of heart tissues was performed. The levels of malondialdehyde (MDA) and glutathione (GSH) in heart tissues were measured. The nuclear factor erythroid 2-related factor 2 (Nrf2) content in nucleus and the proteins of glutathione cysteine ligase catalytic subunit (GCLC) and glutathione cysteine ligase modulatory subunit (GCLM) in heart tissues were assayed by western blotting method.Treatment with Ginsenoside Re at dose of 5, 20 mg/kg reduced troponin T level and CK-MB activity of rats subjected to isoproterenol. The cardioprotective effect of Ginsenoside Re was further confirmed by histopathological examination which showed that Ginsenoside Re attenuated the necrosis and inflammatory cells infiltration. Ginsenoside Re inhibited the increase of MDA content and the decrease of GSH in heart tissues. Moreover, the Nrf2 content in nucleus and the expressions of GCLC and GCLM were significantly increased in the animals treated with Ginsenoside Re.These findings suggested that Ginsenoside Re possesses the property to attenuate isoproterenol-induced myocardial ischemic injury by regulating the antioxidation function in cardiomyocytes.

Study Type : Animal Study, In Vitro Study

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