Objective To explore the regulating mechanism of hepatic injury in obstructive jaundice (OJ). Methods①Rat hepatocytes were isolated by in situ collagenase perfusion and primary culture. Hepatocytes were pretreated with various concentrations of protein kinase C (PKC) agonist parsmeae (PMA) and inhibitor chelerythrine for 20 min. After pretreatment, 50 μmol/L glycochenodeoxycholate (GCDC) was added. Cells were next detected by FCM and TUNEL.②Experimental obstructive jaundice was induced by double ligation of the bile duct (BDL), BDL for 3, 7, 14, 21days.We detected apoptotic status in liver with TUNEL and PKC protein in liver with immunohistochemistry method. Results①PMA increased GCDCinduced apoptosis and chelerythrine decreased GCDCinduced apoptosis in a concentrationdependent manner. ②The apoptotic rate of liver was related to time of OJ. Apoptosis index (AI) was the highest in 14day bile duct ligation. The ber PKC expression, the more number of apoptotic cells in OJ.Conclusion PKC takes part in the regulation and the occurrence and progression of hepatic injury in OJ.