title: Atorvastatin post-conditioning attenuates myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress-related apoptosis.
abstract: 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.
authors.affiliation: *Medical School of Chinese People's Liberation Army, Chinese PLA General Hospital; †Department of Cardiology, Xuanwu Hospital, Capital Medical University; ‡Department of Pathophysiology, Chinese PLA General Hospital; §Department of Pathology, Beijing Chest Hospital, Capital Medical University; and ∥Department of Emergency, Chinese PLA General Hospital, Beijing, China.
authors.forename: Jing-gang
authors.initials: JG
authors.lastname: Xia
authors.forename: Fei-fei
authors.initials: FF
authors.lastname: Xu
authors.forename: Yang
authors.initials: Y
authors.lastname: Qu
authors.forename: Dan-gan
authors.initials: DG
authors.lastname: Song
authors.forename: Hong
authors.initials: H
authors.lastname: Shen
authors.forename: Xiu-hua
authors.initials: XH
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D000069059:Atorvastatin; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use*; D057775:Ischemic Postconditioning; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin