The effect of Bcl-2 adenovirus against murine hepatocyte apoptosis caused by tumor necrosis factor alpha and D-galactosamine.

OBJECTIVE

To evaluate the role of Bcl-2 family proteins in hepatic apoptosis caused by TNF-alpha and D-galactosamine.

METHODS

We induced mouse liver injury with TNF-alpha and D-galactosamine, and detected hepatic apoptosis, the expression of Bcl-2, Bax, and Bak proteins on hepatocytes by using TUNEL or immunohistochemistry, respectively. We also observed the expression of Bcl-2 protein on hepatocytes infected with Bcl-2 adenovirus vector and its protection against hepatocyte apoptosis.

RESULTS

Hepatocyte apoptosis was induced in BalB/c mice pretreated with TNF-alpha plus D-galactosamine, accompanying the enhanced expression of Bax, Bak proteins in hepatocytes. Bcl-2 protein was expressed in murine hepatocytes and lasted at least 1 month after injection of Bcl-2 adenovirus vector, which also lowered ALT level from (1372.9+/-251.4)U/L to (796.5+/-78.7)U/L and reduced hepatocyte apoptosis caused by TNF-alpha and D-galactosamine.

CONCLUSIONS

The enhanced expression of Bax, Bak proteins may play a role in hepatocyte apoptosis induced by TNF-alpha and D-galactosamine. D-galactosamine adenovirus vector can partially reduced hepatocyte apoptosis induced by TNF- alpha and D-galactosamine.