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The antioxidant (-)-epigallocatechin-3-gallate inhibits activated hepatic stellate cell growth and suppresses acetaldehyde-induced gene expression.
Biochem J. 2002 Dec 15; 368(Pt 3):695-704.BJ

Abstract

Activated hepatic stellate cells (HSC) are the primary source of excessive production of extracellular matrix during liver fibrogenesis. Although the underlying mechanisms remain incompletely understood, it is widely accepted that oxidative stress plays a critical role in liver fibrogenesis. Suppression of HSC growth and activation, as well as induction of apoptosis, have been proposed as therapeutic strategies for treatment and prevention of this disease. In the present report, we elucidated, for the first time, effects of the antioxidant (-)-epigallocatechin-3-gallate (EGCG), a major (and the most active) component of green tea extracts, on cultured HSC growth and activation. Our results revealed that EGCG significantly inhibited cultured HSC growth by inducing cell cycle arrest and apoptosis in a dose- and time-dependent manner. In addition, EGCG markedly suppressed the activation of cultured HSC as demonstrated by blocking transforming growth factor-beta signal transduction and by inhibiting the expression of alpha1(I) collagen, fibronectin and alpha-smooth muscle actin genes induced by acetaldehyde, the most active metabolite of ethanol. Furthermore, EGCG reacted differently in the inhibition of nuclear factor-kappaB activity between cultured HSC with or without acetaldehyde stimulation. Taken together, our results indicated that EGCG was a novel and effective inhibitor for activated HSC growth and activation in vitro. Further studies are necessary to evaluate the effect of this polyphenol in prevention of quiescent HSC activation in vivo, and to further elucidate the underlying mechanisms.

Authors+Show Affiliations

Department of Pathology, Louisiana State University Health Sciences Center in Shreveport, Shreveport, LA 71130, USA. achen@lsuhsc.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12223099

Citation

Chen, Anping, et al. "The Antioxidant (-)-epigallocatechin-3-gallate Inhibits Activated Hepatic Stellate Cell Growth and Suppresses Acetaldehyde-induced Gene Expression." The Biochemical Journal, vol. 368, no. Pt 3, 2002, pp. 695-704.
Chen A, Zhang L, Xu J, et al. The antioxidant (-)-epigallocatechin-3-gallate inhibits activated hepatic stellate cell growth and suppresses acetaldehyde-induced gene expression. Biochem J. 2002;368(Pt 3):695-704.
Chen, A., Zhang, L., Xu, J., & Tang, J. (2002). The antioxidant (-)-epigallocatechin-3-gallate inhibits activated hepatic stellate cell growth and suppresses acetaldehyde-induced gene expression. The Biochemical Journal, 368(Pt 3), 695-704.
Chen A, et al. The Antioxidant (-)-epigallocatechin-3-gallate Inhibits Activated Hepatic Stellate Cell Growth and Suppresses Acetaldehyde-induced Gene Expression. Biochem J. 2002 Dec 15;368(Pt 3):695-704. PubMed PMID: 12223099.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The antioxidant (-)-epigallocatechin-3-gallate inhibits activated hepatic stellate cell growth and suppresses acetaldehyde-induced gene expression. AU - Chen,Anping, AU - Zhang,Li, AU - Xu,Jianye, AU - Tang,Jun, PY - 2002/09/11/accepted PY - 2002/09/09/revised PY - 2002/06/10/received PY - 2002/9/12/pubmed PY - 2003/2/11/medline PY - 2002/9/12/entrez SP - 695 EP - 704 JF - The Biochemical journal JO - Biochem J VL - 368 IS - Pt 3 N2 - Activated hepatic stellate cells (HSC) are the primary source of excessive production of extracellular matrix during liver fibrogenesis. Although the underlying mechanisms remain incompletely understood, it is widely accepted that oxidative stress plays a critical role in liver fibrogenesis. Suppression of HSC growth and activation, as well as induction of apoptosis, have been proposed as therapeutic strategies for treatment and prevention of this disease. In the present report, we elucidated, for the first time, effects of the antioxidant (-)-epigallocatechin-3-gallate (EGCG), a major (and the most active) component of green tea extracts, on cultured HSC growth and activation. Our results revealed that EGCG significantly inhibited cultured HSC growth by inducing cell cycle arrest and apoptosis in a dose- and time-dependent manner. In addition, EGCG markedly suppressed the activation of cultured HSC as demonstrated by blocking transforming growth factor-beta signal transduction and by inhibiting the expression of alpha1(I) collagen, fibronectin and alpha-smooth muscle actin genes induced by acetaldehyde, the most active metabolite of ethanol. Furthermore, EGCG reacted differently in the inhibition of nuclear factor-kappaB activity between cultured HSC with or without acetaldehyde stimulation. Taken together, our results indicated that EGCG was a novel and effective inhibitor for activated HSC growth and activation in vitro. Further studies are necessary to evaluate the effect of this polyphenol in prevention of quiescent HSC activation in vivo, and to further elucidate the underlying mechanisms. SN - 0264-6021 UR - https://www.unboundmedicine.com/medline/citation/12223099/The_antioxidant_____epigallocatechin_3_gallate_inhibits_activated_hepatic_stellate_cell_growth_and_suppresses_acetaldehyde_induced_gene_expression_ L2 - https://portlandpress.com/biochemj/article-lookup/doi/10.1042/BJ20020894 DB - PRIME DP - Unbound Medicine ER -