Propofol protects the autophagic cell death induced by the ischemia/reperfusion injury in rats |
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Authors: | Hae Sook Noh Il Woo Shin Ji Hye Ha Young-Sool Hah Seon Mi Baek Deok Ryong Kim |
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Institution: | (1) Department of Molecular and Experimental Medicine MEM-220, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, San Diego, CA 92037, USA; |
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Abstract: | Autophagy has been implicated in cardiac cell death during ischemia/reperfusion (I/R). In this study we investigated how propofol,
an antioxidant widely used for anesthesia, affects the autophagic cell death induced by the myocardial I/R injury. The infarction
size in the myocardium 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. |
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