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Rosuvastatin attenuates infarct size followed myocardial I/R injury through downregulation of mitochondrial-dependent apoptosis

 
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Research Article  
dx.doi.org/10.18081/2333-5106/016-1/19-29
American Journal of BioMedicine Volume 4, Issue 1, pages 19-29
Received November 22, 2015; accepted December 13, 2015; published January 17, 2016 

Terashima Kawasakia, Howard B. Katzb, Kenneth M. Korachb, John D. Couseb mail of corresponding author

Abstract

Rosuvastatin have been reported to prevent complication in patients with myocardial ischemia. However, the mechanism of rosuvastatin in attenuated myocardial injury remains unclear. We investigated the effect of rosuvastatin administration in mice with I/R model. Male C57Bl/6J mice were subjected to myocardial ischemia for 30-min followed by 3-days reperfusion. Rosuvastatin 10 mg/kg or vehicle alone was intraperitoneal administered 15 min before inducing ischemia. Echocardiography at 3-days after myocardial I/R showed higher ejection fraction and stroke volume in mice treated with rosuvastatin compared with vehicle group, whereas left ventricular volumes were comparable. Further, pretreated with rosuvastatin reduced serum levels of CK, LDH, cTn-I, MCP-1 and proinflamatory cytokines, rosuvastatin substantially reduced caspase-3 activity which is a specific indicator of cardiomyocyte apoptosis. The current study was revealed that pretreatment with rosuvastatin attenuated myocardial I/R by inhibiting apoptosis.

Keywords: Rosuvastatin; myocardial injury; myocardial I/R; Apoptosis

Copyright © 2016 by The American Society for BioMedicine and BM-Publisher, Inc.

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