Propofol protects the autophagic cell death induced by the ischemia/reperfusion injury in rats
Propofol protects the autophagic cell death induced by the ischemia/reperfusion injury in rats
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DOI：
10.1007/s10059-010-0130-z
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发表时间：
2010-11-01
影响因子：
3.8
通讯作者：
Kim, Deok Ryong
中科院分区：
文献类型：
--
作者：
Noh, Hae Sook;Shin, Il Woo;Kim, Deok Ryong
自噬与缺血/再灌流(I/R)时心肌细胞死亡有关。在这项研究中，我们研究了被广泛用于麻醉的抗氧化剂异丙酚对心肌I/R损伤诱导的自噬细胞死亡的影响。与未治疗的大鼠相比，异丙酚处理的大鼠在I/R期间心肌梗死范围显著缩小。I/R损伤大鼠心肌细胞内可见大量自噬空泡，而异丙酚处理的I/R损伤大鼠心肌细胞内可见少量自噬空泡。自噬标记物LC3-II在I/R损伤的心肌中表达上调，而在I/R损伤和异丙酚处理的大鼠心肌组织中表达显著下调。此外，异丙酚还抑制I/R诱导的Beclin-1的表达，并促进细胞I/R和Beclin-1/Bcl2相互作用过程中mTOR的磷酸化，从而促进自噬抑制途径。提示异丙酚对心肌I/R损伤所致的自噬细胞死亡有保护作用。
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.