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Apoptosis and Bcl-2 expression in the livers of patients with steatohepatitis.

Authors :
Ramalho RM
Cortez-Pinto H
Castro RE
Solá S
Costa A
Moura MC
Camilo ME
Rodrigues CM
Source :
European journal of gastroenterology & hepatology [Eur J Gastroenterol Hepatol] 2006 Jan; Vol. 18 (1), pp. 21-9.
Publication Year :
2006

Abstract

Objectives: Apoptosis may play a role in the pathogenesis of alcoholic (ASH) and non-alcoholic steatohepatitis (NASH). In this study, we investigated the modulation of apoptosis-related liver proteins in steatohepatitis.<br />Methods: Hepatocyte apoptosis was evaluated by the TUNEL assay in liver tissue of 12 patients with NASH, 12 with ASH and in histologically normal controls. In addition, caspase-3 processing was evaluated by immunoblot analysis. Expression of death receptors, Bcl-2 family members, and NF-kappaB inhibitor (IkappaB) were determined by western blot. Liver biopsies were also graded for inflammation and fibrosis.<br />Results: Apoptotic hepatocytes were markedly increased in NASH (P<0.05) and ASH (P<0.001) as compared to controls. Active caspase-3 was also elevated in steatohepatitis (P<0.01), coinciding with upregulation of pro-apoptotic Bax (P<0.001). Further, production of tumour necrosis factor-receptor 1 was increased up to 4-fold (P<0.05). Degradation of IkappaB increased >70% in steatohepatitis (P<0.001). Notably, Bcl-2 was also strongly expressed (>100-fold; P<0.001). These data were significantly correlated with relative degrees of portal and lobular inflammation.<br />Conclusion: The results show that liver injury in NASH and ASH is associated with apoptosis and NF-kappaB activation. Anti-apoptotic Bcl-2 is strongly expressed, probably reflecting an adaptive response to obesity or alcohol-related stress.

Details

Language :
English
ISSN :
0954-691X
Volume :
18
Issue :
1
Database :
MEDLINE
Journal :
European journal of gastroenterology & hepatology
Publication Type :
Academic Journal
Accession number :
16357615
Full Text :
https://doi.org/10.1097/00042737-200601000-00005