The protective effects of procyanidin supplementation on PM2.5-induced acute cardiac injury in rats.

OBJECTIVE: Numerous epidemiological and experimental studies have indicated that ambient fine particulate matter (PM2.5) exposure can lead to myocardial injury by inhibiting oxidative stress and apoptosis. The effects of procyanidin (PC) on PM2.5-induced cardiovascular diseases (CVDs) are still unknown. The purpose of this study was to explore the protective effect of PC supplementation on PM2.5-induced oxidative stress and cardiomyocyte apoptosis in rats. METHOD: Rats were treated by gavage with three different PC concentrations (50, 100 and 200 mg/kg) for 21 days prior to exposure to 10 mg/kg PM2.5 suspension liquid by intratracheal instillation every other day for three times. We determined myocardial reactive oxygen species (ROS) and malondialdehyde (MDA) levels. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the myocardium were measured. The expression levels of apoptosis-related proteins, including p-Akt/Akt, Bcl-2, caspase-3 and Bax, were determined. In addition, histopathological examination was used to evaluate cardiac injury. RESULTS: PM2.5 exposure noticeably elevated the contents of MDA and ROS and decreased the activities of GSH-Px and SOD. PM2.5 exposure inhibited Bcl-2 expression and up-regulated caspase-3 and Bax expression in the myocardium of rats. The anti-apoptosis-related index p-Akt/Akt was reduced. Moreover, pretreatment with PC could attenuate these PM2.5-induced changes. However, remarkable differences in the protective effect of different PC doses did not exist. CONCLUSIONS: The results indicated that PC supplementation could effectively attenuate the oxidative stress and apoptosis induced by PM2.5 in rat myocardial tissue.