Postconditioning attenuates bile duct cell damage by apoptosis from liver ischemia-reperfusion injury in rats

Abstract

Objective To study the protective effect of postconditioning on bile duct cell damage in the form of apoptosis during liver ischemia-reperfusion (IR) injury by observing the expression of B cell lymphoma/leukemia-2 (bcl-2) and B cell lymphoma/leukemia-2 associated X protein (bax) on bile ducts. Methods Thirty healthy male SD rats were randomly divided into three groups: sham-operation (SO) group, IR group and ischemic postconditioning (IPO) group. IPO was achieved by 6 brief reperfused/ischemia cycles before the persistent reperfusion procedure. The samples of blood and hepatic tissue of all groups were taken after experiment. The activity of γ-glutamyl transpeptidase (GT) in serum was determined. The expression of bcl-2 and bax on bile ducts was detected by immunohistochemistry. The apoptosis index on bile ducts was observed by TdT-mediated dUTP nick end labeling (TUNEL) methods. Results The activity of γ-GT was lower in IPO group [(26.30±3.32) U/L] than that in IR group [(34.64±3.28) U/L] with the difference being statistically significant (P=0.001). As compared with the IR group, the expression of bcl-2 on bile ducts was up-regulated [(77.94±5.25)% vs. (42.67±3.73)%], and that of bax down-regulated [(70.10±4.27)% vs. (90.17±2.12)%] in IPO group, with the difference being statistically significant (P=0.000). As compared with IR group, the apoptosis index in IPO group was decreased [(58.90±2.75)% vs. (79.31±1.12)%, P=0.000], and the pathologically morphologic damages of the bile duct cells were attenuated. Conclusion In the process of liver IR, the postconditioning can promote the expression of bcl-2 and inhibit the expression of bax on bile duct, which may withstand the happening of the bile duct cell apoptosis, thus attenuating the bile duct damage caused by liver IR injury. Key words: Reperfusion injury; Postconditioning; Bile duct; Apoptosis; B cell lymphoma/leukemia-2; B cell lymphoma/leukemia-2 associated X protein