Propofol alleviates hepatic ischemia/reperfusion injury via the activation of the Sirt1 pathway.

BACKGROUND AND OBJECTIVES: Propofol exerts protective effects on multiple organs, including the liver. The aim of the present study was to investigate whether the protective effects of propofol on the liver are related to Sirt1, an NAD+-dependent deacetylase with anti-inflammatory and antioxidant properties. METHODS: After treatment with propofol, hepatic I/R injury was induced in mice. Liver injury, oxidative stress, antioxidant capacity, cytokine production, and apoptotic markers were investigated to assess the effects of propofol pretreatment on hepatic I/R injury. The expression of Sirt1 was assessed by immunohistochemical and western blot analyses, and the expression levels of NF-κB/p65, IκBα, Bcl-2 and Bax were analyzed by western blot. RESULTS: After 70% hepatic I/R injury, the mice that were pretreated with propofol showed considerably less liver injury, enhanced anti-inflammatory and antioxidant capacity, and less apoptosis. Additional studies revealed that propofol pretreatment prior to I/R injury results in reduced NF-κB activation and apoptosis through Sirt1 activation. CONCLUSIONS: The present study is the first to reveal that propofol can significantly reduce hepatic I/R injury by regulating the expression of Sirt1, and these effects may be related to anti-inflammatory and antioxidant effects. Our results suggest that propofol may be an effective therapeutic strategy for the treatment of hepatic I/R injury in hepatobiliary surgery.