[Resistance of Bcl-2 adenovirus vector to HepG(2) cell apoptosis induced by ethanol]

Zhonghua Gan Zang Bing Za Zhi. 2000 Aug;8(4):215-7.
[Article in Chinese]

Abstract

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.

Conclusion: 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.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae / genetics*
  • Animals
  • Apoptosis / drug effects*
  • Cell Line
  • Ethanol / toxicity*
  • Genetic Vectors
  • Humans
  • Liver / drug effects*
  • Liver / pathology
  • Mice
  • Proto-Oncogene Proteins c-bcl-2 / genetics*
  • Proto-Oncogene Proteins c-bcl-2 / physiology

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • Ethanol