Adenoviruses mediated BCL-X1 overexpression protects mice from fulminant hepatic failure.
- Author:
Xiao-an YANG
1
;
Ka ZHANG
;
Xin SHU
;
Hong CAO
;
Qi-huan XU
Author Information
- Publication Type:Journal Article
- MeSH: Adenoviridae; genetics; metabolism; Animals; Apoptosis; Disease Models, Animal; Female; Gene Expression; Genetic Therapy; Genetic Vectors; genetics; metabolism; Humans; Liver; cytology; metabolism; Liver Failure, Acute; genetics; physiopathology; prevention & control; therapy; Rats; Rats, Wistar; bcl-X Protein; genetics; metabolism; therapeutic use
- From: Chinese Journal of Experimental and Clinical Virology 2011;25(2):109-111
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo indentify the relation between hepatic cells apoptosis and the lesion of liver tissue in acute toxic lethal hepatitis.
METHODS60 Wistar mice were randomly divided into normal control, model group and treatment group. Normal control and model group were pretreated by portal vein injection of normal saline, the treatment group was pretreated by portal vein injection of BCL-X1 adenoviruses. The mice of model group and treatment group were received an injection of D-galn and LPS to establish fulminant hepatic failure models 7 days after pretrement. To observe BCL-X1 expression, serum ALT, AST, hepatocyte apoptosis rate, and mortality rate of the three groups.
RESULTSThe BCL-X1 expression was higher in treatment group than in model group; 6 hours after fulminant hepatic failure models were established,the serum ALT, AST level of treatment group was lower than model group;The hepatocyte apoptosis rate of treatment group was lower than model group. The death rate of treatment group was lower than model group.
CONCLUSIONIn fulminant mice hepatic failure models, the hepatocyte apoptosis rate has a positive correlation with death rate, the overexpression of BCL-X1 can decrease the hepatocyte apoptosis rate and the death rate.