Effect and mechanism of propofol in hepatic ischemia/reperfusion injury of rat

摘要

OBJECTIVE: Hepatic ischemia/reperfusion (I/R) injury remains to be one of the most common clinical diseases. This study aimed to explore the potential effect and mechanism of propofol in protecting rat liver from I/R injury. MATERIALS AND METHODS: The hepatic I/R model was established in Sprague-Dawley (SD) rats by perfusing the liver with heparinized cold saline through the portal vein for 20 min. The rats were then received a 100 mg/kg/d propofol administration for the continuously 10 days. The hepatic function indexes of ALT, AST, and GGT were detected by ELISA. The apoptosis of hepatic cells was assessed by TUNEL analysis, and Bax and Bcl-2 expression changes were detected by qRT-PCR and Western blotting. In addition, serum pro-inflammatory factors and the signaling pathway-related protein expressions were detected. RESULTS: Propofol markedly attenuated the increases of ALT, AST, and GGT induced by I/R. Propofol reduced I/R-induced apoptosis and pro-inflammatory factors secretion. Furthermore, propofol could promote the expression of phosphorylated (p)-AKT and inhibited the expression of p-mTOR. CONCLUSIONS: Propofol protects hepatic I/R injury partly by reducing apoptosis and reducing the release of pro-inflammatory cytokines, which is possibly involved in the modulation of the PI3K/AKT/mTOR signaling pathway. All these data suggest that propofol may play certain positive roles in protecting the liver from I/R injury.