Key result
Atorvastatin reduces troponin levels, myocardial inflammation, and apoptosis in viral myocarditis.
Why the study?
The therapeutic efficacy of atorvastatin on Coxsackievirus B3m-induced viral myocarditis was investigated.
Answers are grounded in this paper and cite their sources.
Atorvastatin effects in viral myocarditis remain unproven clinically; leaves open translation from murine models.
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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Sun et al. (2010) studied Coxsackievirus B3m (CVB3m)-induced viral myocarditis. Atorvastatin vs. Untreated virus-challenged mice and Eagle minimal essential medium controls was evaluated on Cardiac troponin I levels, myocardial inflammation, cell apoptosis, and Fas expression (p=<0.05). Atorvastatin altered cardiac troponin I levels and reduced histological severity, apoptosis, and Fas expression in mice with CVB3m-induced myocarditis.
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