title: Atorvastatin attenuates Coxsackie virus B3m-induced viral myocarditis in mice.
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.
authors: Emergency Center of Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
authors: Jian
authors: J
authors: Guan
authors: XiaoLu
authors: X
authors: Sun
authors: Yan
authors: Y
authors: Liang
authors: Wei
authors: W
authors: Dong
authors: LianFeng
authors: L
authors: Zhang
authors: Jun
authors: J
authors: Zhu
authors: GuoGan
authors: G
authors: Wang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects*; D000069059:Atorvastatin; D003384:Coxsackievirus Infections / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D053222:Fas Ligand Protein / Q000378:metabolism; D006538:Heptanoic Acids / Q000627:therapeutic use*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D009205:Myocarditis / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control* / Q000821:virology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D011758:Pyrroles / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D019210:Troponin I / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D053222:Fas Ligand Protein; C491899:Fas protein, mouse; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D012333:RNA, Messenger; D019210:Troponin I; D019014:fas Receptor; D000069059:Atorvastatin