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 language | English |
|---|---|
| Pages (from-to) | 1-8 |
| Number of pages | 8 |
| Journal | Yonsei medical journal |
| Volume | 42 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2001 Jan 1 |
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All Science Journal Classification (ASJC) codes
- Medicine(all)
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Oxidative stress effect on the activation of hepatic stellate cells. / Lee, K. S.; Lee, S. J.; Park, HyoJin; Chung, J. P.; Han, KwangHyub; Chon, C. Y.; Lee, S. I.; Moon, Y. M.
In: Yonsei medical journal, Vol. 42, No. 1, 01.01.2001, p. 1-8.Research output: Contribution to journal › Article
TY - JOUR
T1 - Oxidative stress effect on the activation of hepatic stellate cells.
AU - Lee, K. S.
AU - Lee, S. J.
AU - Park, HyoJin
AU - Chung, J. P.
AU - Han, KwangHyub
AU - Chon, C. Y.
AU - Lee, S. I.
AU - Moon, Y. M.
PY - 2001/1/1
Y1 - 2001/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0035261509&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035261509&partnerID=8YFLogxK
U2 - 10.3349/ymj.2001.42.1.1
DO - 10.3349/ymj.2001.42.1.1
M3 - Article
C2 - 11293487
AN - SCOPUS:0035261509
VL - 42
SP - 1
EP - 8
JO - Yonsei Medical Journal
JF - Yonsei Medical Journal
SN - 0513-5796
IS - 1
ER -