Abstract

Objective To study the role of Ginsenoside Re and Rb3 on mice with viral myocarditis (VMC) and explore the mechanisms. Methods BALB/C mice were infected by coxsackievirus B3 (CVB3) to establish VMC model. The mice were divided into control group, virus group and Ginsenoside Re and Rb3 treatment group (treatment group). On day 5, day 10, day 20 after infection, the level of serum creatine phosphokinase-MB (CK-MB) was detected. Then myocardial sections stained with Masson′s trichrome were used to observe the distribution of mice myocardial collagen fibers, quantify collagen volume fraction (CVF), and detect the levels of superoxide dismutase (SOD). Results (1) The level of CK-MB peaked on day 5, and decreased afterwards[day 5: (463.68±47.62) U/L; day 10: (588.81±56.09) U/L; day 20: (340.48±58.22) U/L, respectively]. While the levels of CK-MB in treatment group were lower than those in virus group[day 5: (378.69±56.02) U/L; day 10: (452.56±67.78) U/L; day 20: (327.13±47.20) U/L, respectively] in the same point. There were significant differences between groups on day 5 and day 10 (P<0.01). (2) In viral group, the blue staining degree gradually increased with time in myocardial sections stained with Masson′s trichrome, especially in myocardial necrosis area. Compared with treatment group, CVF increased significantly in virus group on day 10 and day 20 (day 10: 6.52%±2.34% vs.8.94%±1.67%; day 20: 7.00%±1.53% vs.10.46%±1.74%, P<0.01). The levels of SOD in myocardial sections in virus group were lower than those of control group[day 5: (48.83±17.74) U/L; day 10: (61.41±14.58) U/L; day 20: (66.26±18.97) U/L, respectively, P<0.05], but in treatment group, the level of SOD could be improved significantly[day 5: (72.07±24.85) U/L; day 10: (83.22±19.52) U/L; day 20: (92.00±20.46) U/L, respectively, P<0.05]. Conclusion Because of the inhibition of oxygen radicals and oxidative stress, Ginsenoside Re and Rb3 can protect myocardial tissue. Ginsenoside Re and Rb3 can effectively reduce the extent of myocardial fibrosis. The mechanism may be related with the reduced peroxide level in vivo. Key words: Viral Myocarditis; Coxsackievirus B3; Ginsenoside Re; Ginsenoside Rb3

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