The cardioprotective effects of caffeic acid phenethyl ester (CAPE) on myocardial ischemia/reperfusion (I/R) injury

Reperfusion injury is the acceleration of heart damage which occurs during the reintroduction of coronary blood flow to a prolonged ischemic area [1]. Oxidative stress is a major cause of reperfusion injury by reducing the bioavailability of nitric oxide (NO), damaging cellular function leading to cell death/apoptosis. To date, there is no effective clinical treatment for reperfusion injury. CAPE is an active component of propolis collected from honeybee hives that exhibits both anti-oxidant and anti-inflammatory effects [2]. Recently, CAPE when given prior to ischemia was found to be cardioprotective against I/R injury [3,4]. The beneficial effects of CAPE are possibly mediated by upregulating heme oxygenase-1 and/or increased bioavailability of NO. However, the effects of CAPE when given at reperfusion in myocardial I/R (MI/R) injury has not been evaluated. This study tested the effects of CAPE on postreperfused cardiac function, infarct size, and putative mechanisms in an isolated rat MI/R model when given at reperfusion.