IMR Press / FBL / Volume 19 / Issue 3 / DOI: 10.2741/4224

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Catalase ameliorates hepatic fibrosis by inhibition of hepatic stellate cells activation

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1 Department of Gastroenterology, Shanghai First People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
Academic Editor:Jie Zou
Front. Biosci. (Landmark Ed) 2014, 19(3), 535–541; https://doi.org/10.2741/4224
Published: 1 January 2014
(This article belongs to the Special Issue Immunoregulation and inflammatory disease)
Abstract

Catalase, an endogenous antioxidant enzyme, is thought to have rescue effects on hepatic fibrosis. In this study, the regulation of catalase in CCl₄-induced hepatic fibrogenesis was investigated. Our results indicated that catalase expression was decreased upon CCl₄ treatment in a time-dependent manner, while the expression of several profibrosis and proangiogenic factors, including transforming growth factor (TGF)-beta 1, vascular endothelial growth factor (VEGF), and angiopoietin 1 were significantly increased. To assess the role of catalase in hepatic fibrosis, catalase was overexpressed in HSC-T6 cells. This overexpression resulted in the inhibition of cell proliferation, migratory activity, and alpha-smooth muscle actin (alpha-SMA) expression, key features that characterize activation of hepatic stellate cells (HSC). Overexpression of catalase led to a decrease in the secretion of collagen type 1 and angiopoietin 1. These results indicate that loss of catalase activity is involved in the pathogenesis of hepatic fibrosis caused by the activation of HSCs.

Keywords
ROS
Hepatic Stellate Cells
VEGF
Chronic Liver Diseases
TGF-beta 1
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