BACKGROUND/AIMS: Non-alcoholic steatohepatitis (NASH) is a disorder that is histologically characterized by macrovesicular steatosis and lobular hepatitis with necrosis or ballooning degeneration and fibrosis. NASH can range from a benign condition to end-stage liver disease. The mechanisms promoting transition from steatosis to NASH appear to involve multiple cellular adaptations to the oxidative stress occurring when fatty acid metabolism is altered. We evaluated the relationship between lipid peroxidation and other oxidative stress biomarkers with changes in expression of heme oxygenase-1 (HO-1) in human hepatic steatosis ranging from simple steatosis to NASH. METHODS: HO-1 expression, lipid peroxidation, ferritin and GSH levels were assayed from liver biopsies obtained from 60 subjects: 35 with NASH, 15 with simple steatosis and 10 controls. RESULTS: The HO-1 expression was significantly increased in NASH patients and the increase reflected the severity of the disease. A significant correlation was observed between the increased levels of HO-1 and ferritin, and between the increased levels of HO-1 and lipid peroxidation. Moreover, NASH patients with lower levels of GSH exhibited higher expression of HO-1. CONCLUSIONS: The induction of HO-1 is an adaptive response against oxidative damage elicited by lipid peroxidation and it may be critical in the progression of the disease.
BACKGROUND/AIMS: Non-alcoholic steatohepatitis (NASH) is a disorder that is histologically characterized by macrovesicular steatosis and lobular hepatitis with necrosis or ballooning degeneration and fibrosis. NASH can range from a benign condition to end-stage liver disease. The mechanisms promoting transition from steatosis to NASH appear to involve multiple cellular adaptations to the oxidative stress occurring when fatty acid metabolism is altered. We evaluated the relationship between lipid peroxidation and other oxidative stress biomarkers with changes in expression of heme oxygenase-1 (HO-1) in humanhepatic steatosis ranging from simple steatosis to NASH. METHODS:HO-1 expression, lipid peroxidation, ferritin and GSH levels were assayed from liver biopsies obtained from 60 subjects: 35 with NASH, 15 with simple steatosis and 10 controls. RESULTS: The HO-1 expression was significantly increased in NASH patients and the increase reflected the severity of the disease. A significant correlation was observed between the increased levels of HO-1 and ferritin, and between the increased levels of HO-1 and lipid peroxidation. Moreover, NASH patients with lower levels of GSH exhibited higher expression of HO-1. CONCLUSIONS: The induction of HO-1 is an adaptive response against oxidative damage elicited by lipid peroxidation and it may be critical in the progression of the disease.
Authors: Jeffrey B Schwimmer; Joel E Lavine; Laura A Wilson; Brent A Neuschwander-Tetri; Stavra A Xanthakos; Rohit Kohli; Sarah E Barlow; Miriam B Vos; Saul J Karpen; Jean P Molleston; Peter F Whitington; Philip Rosenthal; Ajay K Jain; Karen F Murray; Elizabeth M Brunt; David E Kleiner; Mark L Van Natta; Jeanne M Clark; James Tonascia; Edward Doo Journal: Gastroenterology Date: 2016-08-26 Impact factor: 22.682
Authors: Jianling Wang; Huaxian Ma; Paul J Boor; V M Sadagopa Ramanujam; G A S Ansari; M Firoze Khan Journal: Free Radic Biol Med Date: 2009-12-04 Impact factor: 7.376
Authors: Giovanni Li Volti; David Sacerdoti; Claudia Di Giacomo; Maria-Luisa Barcellona; Antonio Scacco; Paolo Murabito; Antonio Biondi; Francesco Basile; Diego Gazzolo; Raul Abella; Alessandro Frigiola; Fabio Galvano Journal: World J Gastroenterol Date: 2008-10-28 Impact factor: 5.742