[Resistance of Bcl-2 adenovirus vector to HepG(2) cell apoptosis induced by ethanol].
OBJECTIVE
To evaluate the role of Bcl-2 family proteins in hepatocytic apoptosis caused by ethanol.


METHODS
We induced hepatocytic apoptosis in HepG(2) cells with ethanol and detected the apoptosis with TUNEL assay. Bcl-2, Bax, and Bak protein expression in the hepatocytes was determined by immunohistochemistry method. We also observed the expression of Bcl-2 protein in HepG(2) cells infected with Bcl-2 adenovirus vector and its protection against hepatocytic apoptosis caused by ethanol.


RESULTS
No obvious cytotoxicity was noted in 0.2% and 1% ethanol treatment group, while it developed in 3% ethanol treatment group and accompanied by a marked expression of Bax, Bak proteins.


CONCLUSIONS
The overexpression of Bax, Bak proteins may play a role in HepG(2) cell apoptosis induced by ethanol and can be blocked effectively by Bcl-2 adenovirus vector.
Zhang
B
B
Institute of Viral Hepatitis, Chongqing University of Medical Sciences, Chongqing 400010, China.
Zhang
D
D
Ren
H
H
D000256:Adenoviridae / Q000235:genetics*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D000431:Ethanol / Q000633:toxicity*; D005822:Genetic Vectors; D006801:Humans; D008099:Liver / Q000187:drug effects* / Q000473:pathology; D051379:Mice; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics* / Q000502:physiology
D019253:Proto-Oncogene Proteins c-bcl-2; D000431:Ethanol