Propofol is an intravenous anesthetic, reported to have a protective effect against ischemia/reperfusion (I/R) injury in heart and brain, but no definite data are available concerning its effect in hepatic I/R. This work investigated the effect of propofol anesthesia on hepatic I/R injury using in vivo rat model. Four groups of rats were included: sham operated, I/R (30？min ischemia and 2？h reperfusion), I/R treated with propofol (10？mg/kg/h), and I/R treated with propofol (20？mg/kg/h). Liver enzyme leakage, TNF-α and caspase-3 levels, and antiapoptotic Bcl-xL/apoptotic Bax gene expression, together with histopathological changes, were used to evaluate the extent of hepatic I/R injury. Compared with sham-operated group, I/R group showed significant increase in serum levels of liver enzymes (ALT, AST), TNF-α, and caspase-3 and significant decrease in the Bcl-xL/Bax ratio, associated with histopathologic damage in liver. Propofol infusion significantly attenuated these changes with reduced hepatic histopathologic lesions compared with nonpreconditioned I/R group. However, no significant differences were found between two groups treated with different doses of propofol. In conclusion, propofol infusion reduced hepatic I/R injury with decreased markers of cellular apoptosis. Therefore, propofol anesthesia may provide a useful hepatic protection during liver surgery. 1. Introduction Liver ischemia/reperfusion (I/R) injury is a common pathophysiological process prevalent in hepatic transplant surgery, partial hepatectomy, and shock conditions. Liver failure induced by I/R is the most serious complication with a direct impact on prognosis of the disease and even causes deaths [1]. This accounts for about 80% of liver transplant failures and the high mortality rate after partial hepatectomy [2]. Several mechanisms interact during I/R to cause liver damage and death of liver cells, including the direct ischemic cellular damage as well as cell injury due to activation of inflammatory response after reperfusion [1]. Apoptosis is recognized as the key feature of cell death in the ischemic liver [3]. Apoptosis (programmed cell death) is an active process characterized by cell shrinkage, chromatin condensation, nuclear fragmentation, and formation of apoptotic bodies [4]. On the other hand, necrosis is passive and characterized by cell swelling, rupture of the plasma membrane, and cell lysis, with leakage of cytoplasmic components [5]. Cellular apoptosis was shown to be mediated by a family of cysteine aspartate (caspases) caspase-1 to caspase-14. The poly
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