Apoptosis of hepatocytes and the expression of Bax and Bcl-2 in nonalcoholic steato-hepatitis in rat
- VernacularTitle:非酒精性脂肪性肝炎肝细胞凋亡及凋亡相关蛋白的表达
- Author:
Jing ZHANG
;
Jingmin ZHAO
;
Guangde ZHOU
- Publication Type:Journal Article
- Keywords:
apoptosis;
nonalcoholic steatohepatitis;
Bax;
Bcl-2;
immunohistochemistry
- From:
Medical Journal of Chinese People's Liberation Army
1983;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the apoptotic changes in hepatocytes and the expression of apoptosis-associated proteins Bax and Bcl-2 in the liver tissue of a rat nonalcoholic steato-hepatitis (NASH) model, and explore the relationship between hepatocyte apoptosis and the degree of NASH pathological changes. Methods A rat model of NASH was reproduced with feeding a fat-rich diet for a period of 2, 4, 6, 8 and 12 weeks. Cells apoptosis was evaluated by TdT-mediated dUTP nick end labeling (TUNEL), and the expression of Bax and Bcl-2 proteins was detected by immunohistochemistry in rat liver tissue of control and model groups respectively. Results The number of TUNEL-positive cells was increased in the second week, peaking at the 8th week, and it was significantly correlated with steatosis and hepatic fibrosis (r=0.707 and 0.750, respectively, P0.05). The expressions of Bax and Bcl-2 proteins were mainly located in cytoplasm of hepatocytes, some of which contained lipid droplets. Bax and Bcl-2 positive cells increased gradually with the progression of NASH. In early stage of modeling, the number of Bax positive cells was greater than that of Bcl-2, but the number of the both proteins tended to be about same in the late stage of modeling. Conclusion The cell apoptosis is a main pattern of liver damage in the process of NASH, and it is closely associated with the pathological changes. Proapoptosis protein Bax and antagonisitic protein Bcl-2 might participate in the modulation of hepatocytes apoptosis in the early stage of NASH, and they also have a marked effect in the whole process of NASH.
