Oxidative stress effect on the activation of hepatic stellate cells.

K. S. Lee, S. J. Lee, H. J. Park, J. P. Chung, K. H. Han, C. Y. Chon, S. I. Lee, Y. M. Moon

Research output: Contribution to journalArticle

73 Citations (Scopus)

Abstract

Collagen is the most excessive extracellular matrix protein in hepatic fibrosis. Activated, but not quiescent, hepatic stellate cells (HSCs) have a high level of collagen and a smooth muscle actin (alpha SMA) expression. HSCs play a key role in the pathogenesis of hepatic fibrosis. We analyzed a mechanism leading to HSC activation by evaluating the role of oxidative stress and the expression of NFkB. In vitro study HSCs were proliferated (PCNA:2% vs 68%) and activated (alpha SMA: 5% vs 78%) by ascorbate/FeSO4, and HSCs activated by type I collagen were blocked (PCNA: 97% vs 4%, a SMA: 86% vs 9%) by a-tocopherol. In vivo study means of a SMA positive cells in liver at 400 x HPF were 48.3+/-5.2 and 15.2+/-1.8 and [3H]thymidine uptake of HSC was 529.2+/-284.8 cpm and 223.0+/-86.3 cpm in control and a-tocopherol treated group respectively at 32 hours after CCl4 injection. Nuclear extracts from activated, but not from quiescent, HSCs formed a complex with the NFkB cognate oligonucleotidesand alpha-tocopherol inhibited this bindings. This study indicates that oxidative stress plays an essential role through the induction of NFkB on HSC activation.

Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalYonsei medical journal
Volume42
Issue number1
DOIs
Publication statusPublished - 2001 Feb

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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