α-Lipoic acid inhibits liver fibrosis through the attenuation of ROS-triggered signaling in hepatic stellate cells activated by PDGF and TGF-β

doi:10.1016/j.tox.2011.01.009

CNU IR > Pharmacy and Science > Dept. of Biotechnology (including master's program) > Periodical Articles > Item 310902800/26697

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Title:	α-Lipoic acid inhibits liver fibrosis through the attenuation of ROS-triggered signaling in hepatic stellate cells activated by PDGF and TGF-β
Authors:	Foo, Ning-Ping Lin, Shu-Huei Lee, Yu-Hsuan Wu, Ming-Jiuan Wang, Ying-Jan
Contributors:	生物科技系
Keywords:	α-Lipoic acid Dihydrolipoic acid Liver fibrosis Reactive oxygen species Hepatic stellate cell
Date:	2011-03
Issue Date:	2013-06-05 16:42:53 (UTC+8)
Publisher:	Elsevier
Abstract:	Reactive oxygen species (ROS) have been implicated in hepatic stellate cell activation and liver fibrosis. We previously reported that α-lipoic acid (LA) and its reduced form dihydrolipoic acid (DHLA) inhibited toxicant-induced inflammation and ROS generation. In the present study, we further examined the effects of LA/DHLA on thioacetamide (TAA)-induced liver fibrosis in rats and the possible underlying mechanisms in hepatic stellate cells in vitro. We found that co-administration of LA to rats chronically treated with TAA inhibited the development of liver cirrhosis, as indicated by reductions in cirrhosis incidence, hepatic fibrosis, and AST/ALT activities. We also found that DHLA inhibited TGF-β/PDGF-stimulated HSC-T6 activation and ROS generation. These effects could be mediated by the MAPK and PI3K/Akt pathways. According to our current results, LA may have a beneficial role in the treatment of chronic liver diseases caused by ongoing hepatic damage. Abbreviations HSCs, hepatic stellate cells; ROS, reactive oxygen species; α-SMA, α-smooth muscle actin; PDGF, platelet-derived growth factor; TGF-β, transforming growth factor-β; LAα-, lipoic acid; DHLA, dihydrolipoic acid; MAPK, mitogen-activated protein kinase; ERK, extracellular signal-regulated kinase; JNK, c-jun N-terminal kinase; PI3K/Akt, phosphatidylinositol 3-kinase/amino kinase terminal; TAA, thioacetamide; ALT, alanine aminotransferase; AST, aspartate aminotransferase
Relation:	Toxicology 282(1-2), pp.39-46
Appears in Collections:	[Dept. of Biotechnology (including master's program)] Periodical Articles

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