The bcl-2 mRNA expression in GCDC-induced obstructive jaundice in rats and its implication in hepatocellular apoptosis.
- Author:
Jianming WANG
1
;
Shengquan ZOU
Author Information
1. Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Cholestasis, Extrahepatic;
chemically induced;
metabolism;
pathology;
Glycochenodeoxycholic Acid;
Hepatocytes;
metabolism;
pathology;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
genetics;
RNA, Messenger;
biosynthesis;
genetics;
Rats;
Rats, Wistar
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2002;22(1):34-36
- CountryChina
- Language:English
-
Abstract:
The modulatory role of bcl-2 gene in hepatocellular apoptosis of rats with glycochenodeoxycholate (GCDC)-induced obstructive jaundice was investigated. The hepatocytes in normal rats and those with bile duct-ligation for 7 days, 14 days and 21 days were isolated and obtained by in situ collagenase perfusion and primary culture. The expression of bcl-2 mRNA in the hepatocytes was detected by RT-PCR. Primary culture was performed on the hepatocytes from normal rats and those with bile duct-ligation for 14 days. 100 mumol/L GCDC was added to the hepatocytes for incubation for 24 h. The hepatocellular apoptotic ratio was measured by using FCM and hepatocellular apoptosis detected in situ by using TUNEL technique. Results showed that the expression of bcl-2 mRNA was not detectable in the hepatocytes of normal rats by RT-PCR technique, while detectable in the hepatocytes of those with bile duct ligation (BDL) for 7, 14 and 21 days. Hepatocellular apoptosis in the BDL group was obviously decreased as compared with normal control group after addition of 100 mumol/L GCDC to the cells for 24 h. It was concluded that the hepatocytes in the BDL rats expressed bcl-2. During obstructive jaundice, expression of bcl-2 from the hepatocytes can inhibit the bile salt-induced hepatocellular apoptosis.