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Attenuation of hepatic fibrosis by an imidazolium salt in thioacetamide-induced mouse model.

Abstract：

BACKGROUND AND AIM:Hepatic fibrosis is a worldwide healthy burden associated with significant morbidity and mortality. It is caused by a variety of chronic liver injuries. There is currently no effective treatment for liver fibrosis. In this report, we tested an imidazolium salt, 1,3-diisopropylimidazolium tetrafluoroborate (DPIM), for its anti-fibrotic properties in the thioacetamide-induced mouse model. METHODS:DPIM was orally delivered to the thioacetamide-treated mice via drinking water for 12 weeks at the onset of thioacetamide treatment at a concentration of 0.1% (prevention group), and for 4 weeks starting at the 8(th) week at a concentration of 0.1% or 0.2% (attenuation group), respectively. Messenger RNA and protein were determined by real-time polymerase chain reaction and Western blotting, matrix metalloproteinase (MMP) activities were measured by fluorogenic peptide substrate and zymography. Mitogen-activated protein kinase (MAPK) and PI3K inhibitors were applied in HSC-T6 cells in combination of DPIM to probe possible signal pathways underlying the compound's action. RESULTS:We observed a significant reduction in collagen deposition in both prevention and attenuation groups. The α-smooth muscle actin (SMA) and transforming growth factor (TGF)-β gene expressions were also reduced in both groups. The reduction of collagen deposition could be in part attributed to the suppression of CCR-2 expression and the enhanced matrix protein remodeling by metalloproteinases, especially MMP-3. MAPK and PI3K signaling pathways may be partially participated in DPIM's molecular action. CONCLUSION:DPIM reduced fibrosis in the thioacetamide-induced mouse liver fibrosis model, and warranted further studies for possible clinical application in the future.

journal_name

J Gastroenterol Hepatol

journal_title

Journal of gastroenterology and hepatology

authors

Ding Z,Zhuo L

doi

10.1111/j.1440-1746.2012.07265.x

subject

Has Abstract

pub_date

2013-01-01 00:00:00

pages

188-201

issue

1

eissn

0815-9319

issn

1440-1746

journal_volume

28

pub_type

杂志文章

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