The effects of 17-β estradiol on hepatocyte apoptosis and expression of Bcl-2 and Bax in the liver-resected-rats with ischemia reperfusion injury / 中华肝胆外科杂志

ABSTRACT

Objective To investigate the effects of 17-β estradiol on hepatocyte apoptosis and the expression of Bcl-2 and Bax in hepatic tissue after reduced-size ischemia reperfusion injury and its mechanism in liver protection.Methods A rat model of reduced-size hepatic ischemia-reperfusion injury was established in 75 male Sprague-Dawley rats.They were randomly allocated into three groupsSham group,ischemia-reperfusion(IR)group,and 17-β estradiol(E2 + IR)group.Liver functions,liver histology and hepatocellular apoptosis rates were observed after reperfusion.Hepatocellular ap optosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)method and the expression of Bcl-2 and Bax were determined by Western blotting.Results The levels of ALT and AST were higher and peaked after 12 h of reperfusion in the IR group compared with the sham group.The histological changes in the liver of the IR group consisted of hepatocyte swelling,hepatic sinusoids narrowing,inflammatory cell infiltration and hepatocyte necrosis in some areas of the livers.The IR group also exhibited an increased rate of hepatocellular apoptosis at 12 h after reperfusion.The protein expression of Bcl-2 decreased while the expression of Bax increased.In the 17-β estradiol group,the levels of ALT and AST were lower,the pathological changes were milder and the rate of hepatocellular apoptosis was lower at 12 h in comparison to those of the IR group.The expression of Bcl-2 was higher and the expression of Bax was lower in the 17-β estradiol group in comparison to those of the IR group.Conclusions 17-β estradiol can relieve the hepatic ischemia reperfusion injury in rat livers.17-β estradiol may inhibit apoptosis in hepatic tissue by up regulating Bcl-2 and down-regulating Bax,thus producing a protective effect on hepatic ischemia-reperfusion injury.