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- W2227887435 abstract "Aims：Recent evidences indicate that obesity progress some hepatic diseases characterized progressive fibrosis involving the hepatic renin−angiotensin system, so−called nonalcoholic fatty liver disease（NAFLD）or nonalcoholic steatohepatitis（NASH）.Main methods：We evaluated the effects of telmisartan on the transforming growth factor（TGF）−β−induced activation of the human hepatic stellate cell line, LX2 cells, by measurement of the regulation of angiotensin I I type 1 receptor（AT1−R）and peroxisome proliferator−activated receptor−γ（PPARγ）mRNA and quantifying the markers of the hepatic fibrosis, such as α1 procollagen, α−smooth muscle actin（αSMA）, and matrix metalloproteinase 13（MMP13）mRNA, using quantitative real time PCR analysis.Key findings：Both telmisartan and losartan suppressed some TGF−β−induced fibrotic markers, such as α1 procollagen, αSMA, and MMP13 mRNA, and AT1−R mRNA,and increased in TGF−β1−decreased PPARγ mRNA in LX2 cells. The effects on expression of α1 procollagen and αSMA mRNA and rapid suppression of MMP13 mRNA by telmisartan, which antagonizes AT1−R and activates PPARγ, compared with those of losartan indicate that the combined property of telmisartan may be more effective on hepatic fibrosis than blockade of AT1−R alone.Significance：The present results show that telmisartan may ameliorate hepatic fibrosis induced by obesity in addition to the effects by blockade of AT1−R alone and be an alternative choice of the treatment for hepatic fibrotic diseases related to obesity, such as NAFLD and NASH." @default.
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- W2227887435 date "2009-01-01" @default.
- W2227887435 modified "2023-09-24" @default.
- W2227887435 title "Blockade of angiotensin II type 1 receptor by telmisartan suppressed activation of human hepatic stellate cells" @default.
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