| Objective:The goal of the study was to investigate the therapeutic benefits of trimetazidine on viral myocarditis in Balb/c mice.Method:Coxsackie virus B3m-induced myocarditis in Balb/c mice was studied.274male4-6week-old Balb/c mice were divided into five groups randomly, including normal group (n=32), virus group (n=80), trimetazidine control group (n=26, mice were administered trimetazidine10mg/kg/day only), low dose group (n=69, mice were administered trimetazidine10mg/kg/day) and high dose group (n=67, Mice were administered trimetazidine20mg/kg/day). The mice in the nomal group and trimetazidine control group were administered intraperitoneally with Eagle’s minimal essential medium0.4ml per mouse; The mice in the virus group, low dose group and high dose group were inoculated intraperitoneally with virus CVB3m0.4ml×1×103PFU/mL per mouse. Trimetazidine was given3days after viral challenge and treatment lasted for14days in the trimetazidine control group, low dose group and high dose group. The mice in nomal group and virus group were administered the same volume water. Effects of trimetazidine on survival rate and myocardial inflammation were studied. Blood and Myocardial tissue samples were collected for the level of cardiac troponin I (cTnI), superoxide dismutase (SOD) and maleic dialdehyde (MDA) detection on days3,7,10,14and21after virus inoculation (the same days for the nomal group and trimetazidine control group). Fas mRNA expression was detected by Real-time PCR.Results:The mice in the infected groups occurred symptoms such as eating less, drinking less and weight loss at3days post-inoculation. Then the symptoms gradually get worse, mice began to die on the fourth day and days4-10were the death peak. The survival rate in the high dose group was better than in virus group (P=0.008).From the seventh day obvious pathological changes can be observed with the light microscope. The myocardial histopathological score of mice in each infected group on day7-21after infection were significantly higher than that in normal group, H&E staining revealed significant improvement of quantitative pathological features in the trimetazidine treatment group. The differences in cTnI values between the virus group and trimetazidine treatment groups achieve statistical significance, there was decrease in cTnl in the trimetazidine treatment groups (P<0.05). There were differences in the values of SOD and MDA between the virus group and trimetazidine treatment groups.The content of MDA was significantly decreased (P<0.05) and the activity of SOD was increased especially (P<0.05) in the trimetazidine treatment groups. Real-time PCR revealed that the virus induced marked increases in Fas mRNA expression, which could be prevented by treatment with trimetazidine. High dose group more obviously improve the above indexes compared with low dose group.Conclusion:These results demonstrate that Trimetazidine can improve survival rates and reduces the histological severity of CVB3m-induced myocarditis. The therapeutic benefits of Trimetazidine on myocarditis may be explained by its antioxidant activity and inhibition of fas signal transduction pathway. Objective:The goal of this study was to investigate the therapeutic benefits of high dose of of prednisone on viral myocarditis in Balb/c mice. Discussion the difference between different dose of prednisone on viral myocarditis in mice at the medication.Method:Coxsackie virus B3m-induced myocarditis in Balb/c mice was studied. One male4-6week-old Balb/c mice were divided into four groups randomly, including control group (n=32, mice were administered Eagle’s minimal essential medium), virus group (n=25,virus solution intraperitoneally,0.4×1×103PFU/mL), low dose group (n=21, mice were administered prednisone lmg/kg/day), high dose group (n=22, mice were administered prednisone10mg/kg/day). Prednisone was given3days after viral challenge and treatment lasted for14days in the prednisone treatment groups. The mice in control group and virus group were administered the same volume water. Effects of prednisone on survival rate and myocardial inflammation were studied. Blood samples were collected for cardiac troponin I detection on days3,7and14after virus inoculation. Fas mRNA expression were detected by Real-time PCR.Results:The mice in the infected group occurred symptoms such as eating less, drinking less and weight loss at3days post-inoculation. Then the symptoms gradually get worse, mice began to die on the fourth day and days4-10were the death peak. Prednisone treatment can not improve survival rates compared with virus group. Since the seventh day, obvious pathological changes can be observed with the light microscope. The myocardial histopathological score of mice in three infected groups on days7、14after infection were significantly higher than that in control group, H&E staining revealed significant improvement of quantitative pathological features in the Prednisone treatment groups (P<0.05). The differences in cTnI values between the virus group and prednisone treatment groups achieve statistical significance, there was decrease in cTnI in the prednisone treatment groups (P<0.01). Real-time PCR revealed that the virus induced marked increases in Fas mRNA expression (P<0.05), which could be prevented by treatment with prednisone. There were no better effects of high dose of prednisone on the above indexes compared with low dose of prednisone treatment.Conclusion:The treatment of viral myocarditis with different doses of prednisone in mice, can not improve the survival rate of mice with viral myocarditis. Prednisone therapy reduced the inflammatory infiltration in myocardium, inhibited autoimmune response. But there were no better therapeutic effects of high dose of prednisone on myocarditis compared with low dose of prednisone treatment. It may be that prednisone have better effect on viral myocarditis with the appropriate dose at the appropriate time. |
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