Atorvastatin post-conditioning attenuates myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress-related apoptosis.

The present study examined whether atorvastatin, when used for pharmacological postconditioning, attenuated myocardial ischemia-reperfusion (I/R) injury in a manner similar to ischemic postconditioning (I-PostC), that is, by inhibition of endoplasmic reticulum (ER) stress-related apoptosis. In the present study, markers for myocardial injury, infarct area, and hemodynamics, and indicators of ER stress and apoptosis were compared in ischemic and atorvastatin-induced postconditioning as a means of evaluating the protective effect of atorvastatin postconditioning in I/R injury and whether, as in I-PostC, inhibition of ER stress is involved. Both ischemic and atorvastatin-mediated postconditioning significantly decreased indications of cardiac damage and reduced serum concentrations of markers for myocardial injury, reduced the infarct area seen at the end of reperfusion, and improved left ventricular systolic function. We found that high-dose atorvastatin- and I-PostC significantly downregulated expression of glucose-regulating protein 78 and calreticulin (CRT; ER stress markers), expression of C/EBP homologous protein (CHOP), and caspase 12 (markers for ER stress-related apoptosis), and Bax (downstream molecule of CHOP), in the myocardial area at risk. Atorvastatin and I-PostC have similar cardioprotective effects in I/R injury and inhibit the ER stress-related apoptotic pathway.