Yunfeng Xiao1, Tianlong Liu2, Xiaoling Liu3, Lanbin Zheng4, Dongsheng Yu4, Yuanyan Zhang1, Xinyu Qian1, Xiaolei Liu1. 1. Department of Pharmacology, Inner Mongolia Medical University, Hohhot 010110, China. 2. Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, China. 3. Department of Pharmacy, Inner Mongolia People's Hospital, Hohhot 010017, China. 4. Department of Psychiatry, Inner Mongolia Mental Health Center, Hohhot 010010, China.
Abstract
BACKGROUND: To investigate the therapeutic effect of total Astragalus saponins (AST) against viral myocarditis in animal and cell models. METHODS: Primary myocardiocytes (PMCs) were stimulated by the coxsackie B (CVB) 3 virus to prepare the cell model of viral myocarditis. Cell viability, apoptosis and the mRNA expression of C-Myc, tumor necrosis factor (TNF)-α and Fas were detected to evaluate the protective effects of AST on CVB3-induced PMC damage. RESULTS: AST could significantly increase survival and decrease the ratio of heart weight: body weight (P<0.05). The level of myocardial fibrosis in the AST group was significantly lower than that in the CVB3 group. Compared with the CVB3 group, the ejection fraction was increased significantly in the AST group. Levels of lactate dehydrogenase and creatine kinase-MB in the peripheral blood of the AST group were significantly lower than those in the control group. In vitro, AST could significantly decrease CVB3-induced PMC apoptosis. Expression of C-Myc, TNF-α, Fas in the AST group was significantly lower than that in the CVB3 group. CONCLUSIONS: It is demonstrated that AST was protective against CVB3-induced viral myocarditis, which may be associated with a decrease in CVB3-induced apoptosis and down-regulation of expression of C-Myc, TNF-α and Fas.
BACKGROUND: To investigate the therapeutic effect of total Astragalus saponins (AST) against viral myocarditis in animal and cell models. METHODS: Primary myocardiocytes (PMCs) were stimulated by the coxsackie B (CVB) 3 virus to prepare the cell model of viral myocarditis. Cell viability, apoptosis and the mRNA expression of C-Myc, tumor necrosis factor (TNF)-α and Fas were detected to evaluate the protective effects of AST on CVB3-induced PMC damage. RESULTS: AST could significantly increase survival and decrease the ratio of heart weight: body weight (P<0.05). The level of myocardial fibrosis in the AST group was significantly lower than that in the CVB3 group. Compared with the CVB3 group, the ejection fraction was increased significantly in the AST group. Levels of lactate dehydrogenase and creatine kinase-MB in the peripheral blood of the AST group were significantly lower than those in the control group. In vitro, AST could significantly decrease CVB3-induced PMC apoptosis. Expression of C-Myc, TNF-α, Fas in the AST group was significantly lower than that in the CVB3 group. CONCLUSIONS: It is demonstrated that AST was protective against CVB3-induced viral myocarditis, which may be associated with a decrease in CVB3-induced apoptosis and down-regulation of expression of C-Myc, TNF-α and Fas.
Authors: F C Kischkel; D A Lawrence; A Tinel; H LeBlanc; A Virmani; P Schow; A Gazdar; J Blenis; D Arnott; A Ashkenazi Journal: J Biol Chem Date: 2001-10-02 Impact factor: 5.157