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Published on: July 15, 2019
Atorvastatin attenuates Coxsackie virus B3m-induced viral myocarditis in mice
Jian Guan1, XiaoLu Sun, Yan Liang
1Emergency Center of Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Insights
Atorvastatin effectively treats Coxsackievirus B3m-induced myocarditis in mice, reducing inflammation, apoptosis, and improving cardiac function. This study highlights its therapeutic potential for viral heart infections.
Area of Science:
- Cardiology
- Virology
- Pharmacology
Background:
- Myocarditis is inflammation of the heart muscle, often caused by viral infections like Coxsackievirus B3.
- Current treatments for viral myocarditis are limited, necessitating the exploration of novel therapeutic agents.
Purpose of the Study:
- To evaluate the therapeutic efficacy of atorvastatin in a mouse model of Coxsackievirus B3m-induced myocarditis.
- To investigate the effects of atorvastatin on myocardial inflammation, apoptosis, and Fas expression.
Main Methods:
- Mice were infected with Coxsackievirus B3m and treated with atorvastatin starting 3 days post-infection for 14 days.
- Echocardiography, cardiac troponin I analysis, histology, immunohistochemistry, RT-PCR, and Western blotting were employed to assess therapeutic effects.
Main Results:
- Atorvastatin treatment significantly improved pathological features, reduced cardiac cell apoptosis, and decreased myocardial inflammation.
- Cardiac troponin I levels were significantly lower in atorvastatin-treated mice compared to untreated controls.
- Atorvastatin reversed virus-induced increases in Fas messenger RNA and protein expression.
Conclusions:
- Atorvastatin demonstrates significant therapeutic efficacy in reducing the severity of Coxsackievirus B3m-induced myocarditis.
- The drug inhibits apoptosis and Fas expression in the myocardium, suggesting a protective mechanism against viral-induced heart damage.
Abstract:
In the present study, we determined the therapeutic efficacy of atorvastatin on Coxsackievirus B3m (CVB3m)-induced myocarditis. Mice were administered Eagle minimal essential medium, virus solution, atorvastatin, or virus plus atorvastatin. Atorvastatin was given 3 days after viral challenge, and the treatment lasted for 14 days. On days 3, 7, 10, 14, 21, and 30 after virus inoculation (same days for the atorvastatin only group), echocardiograms were performed, and blood samples were collected for cardiac troponin I analysis. Myocardial inflammation, cell apoptosis, and Fas expression were detected by histology and immunohistochemistry. Hematoxylin and eosin staining and transmission electron microscopy revealed significant improvement of quantitative pathological features in the CVB3m-infected group treated with atorvastatin. Immunohistochemistry also showed a marked decrease in apoptosis of cardiac cells in the atorvastatin-treated group compared with infected animals without treatment. The differences in the values of cardiac troponin I between the atorvastatin treated and untreated virus-challenged mice were statistically significant (P < 0.05). Reverse transcription-polymerase chain reaction and western blotting revealed that the virus induced marked increases in Fas messenger RNA and protein expression, which was reversed by atorvastatin. These results demonstrate that atorvastatin reduces the histological and functional severity of CVB3m-induced myocarditis and inhibits apoptosis and Fas expression in the myocardium of type B Coxsackie virus-infected mice.
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