Autophagy has been implicated in cardiac cell death dur-ing ischemia/reperfusion (I/R). In this study we investi-gated how propofol, an antioxidant widely used for anes-thesia, affects the autophagic cell death induced by the myocardial I/R injury. The infarction size in the myocar-dium was dramatically reduced in rats treated with propofol during I/R compared with untreated rats. A large number of autophagic vacuoles were observed in the cardiomyocytes of I/R-injured rats but rarely in I/R-injured rats treated with propofol. While LC3-II formation, an autophagy marker, was up-regulated in the I/R-injured myocardium, it was significantly down-regulated in the myocardial tissues of I/R-injured and propofol-treated rats. Moreover, propofol inhibited the I/R-induced expression of Beclin-1, and it accelerated phosphorylation of mTOR during I/R and Beclin-1/Bcl-2 interaction in cells, which indicates that it facilitates the inhibitory pathway of autophagy. These data suggest that propofol protects the autophagic cell death induced by the myocardial I/R injury.

Keywords: autophagy, Beclin-1/Bcl-2 interaction, cell death, ischemia/reperfusion, propofol