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.
Zhang
B
B
Viral Hepatitis Institute of Chongqing University of Medical Sciences, Chongqing 400010, China.
Zhang
D
D
Ren
H
H
Ma
Y
Y
D000256:Adenoviridae / Q000235:genetics*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D005688:Galactosamine / Q000494:pharmacology*; D005822:Genetic Vectors; D022781:Hepatocytes / Q000187:drug effects* / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha; D005688:Galactosamine