Pinocembrin reduces cardiac arrhythmia and infarct size in rats subjected to acute myocardial ischemia/reperfusion

Author： Lungkaphin Anusorn Pongchaidecha Anchalee Palee Siripong Arjinajarn Phatchawan Pompimon Wilart Chattipakorn Nipon

Publisher： NRC Research Press

ISSN： 1715-5312

Source： Applied Physiology, Nutrition, and Metabolism, Vol.40, Iss.10, 2015-01, pp. : 1031-1037

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Abstract

Oxidative stress plays an important role in the pathogenesis of ischemia/reperfusion (I/R) injury induced by cardiac dysfunction. Pinocembrin (5,7-dihydroxyflavanone) is a flavonoid found in propolis and in rhizomes of fingerroot (Boesenbergia pandurata) that is reported to have pharmacological properties including antimicrobial, antioxidant, and anti-inflammatory activities. The cardioprotective effects of pinocembrin in an I/R model were investigated in this study. Male Wistar rats (n = 20) were randomly divided into 2 groups to receive either pinocembrin (30 mg/kg body weight) or the vehicle intravenously. Thirty minutes later, the left anterior descending coronary artery of each rat was ligated for 30 min, and then reperfusion was allowed for 120 min. Cardiac function improved in the pinocembrin-treated group: the time to first ventricular fibrillation (VF) was significantly longer in the treated group (550 ± 54 s) than in the vehicle-only control group (330 ± 27 s) (p < 0.05). VF incidence and arrhythmia score were lower and infarcts were 49% smaller in the pinocembrin-treated group than in the control group (p < 0.05). In the pinocembrin-treated group, malondialdehyde levels and Bax/Bcl-2 ratios decreased, and the ratio of phosphorylated connexin 43 (phospho-Cx43) to total Cx43 increased in infarcted tissues compared with the non-infarcted area (p < 0.05). Pinocembrin exhibited cardioprotective effects during I/R, evidenced by improved cardiac function, fewer arrhythmias, and smaller infarcts in treated hearts than in controls. These benefits may be due to pinocembrin’s antiapoptotic and anti-oxidative stress effects and its ability to increase the phosphorylation of Cx43 in ischemic myocardium.