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|標題: ||α-Lipoic acid inhibits liver fibrosis through the attenuation of ROS-triggered signaling in hepatic stellate cells activated by PDGF and TGF-β|
|作者: ||Foo, Ning-Ping|
|關鍵字: ||α-Lipoic acid|
Reactive oxygen species
Hepatic stellate cell
|上傳時間: ||2013-06-05 16:42:53 (UTC+8)|
|摘要: ||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.
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
|關聯: ||Toxicology 282(1-2), pp.39-46|
|Appears in Collections:||[生物科技系(所)] 期刊論文|
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