Effect of ligand of peroxisome proliferator-activated receptor γ on the biological characters of hepatic stellate cells

AIM： To study the effect of rosiglitazone, which is a ligand of peroxisome proliferator-activated receptor gamma （PPARy）, on the expression of PPARy in hepatic stellate cells （HSCs） and on the biological characteristics of HSCs. METHODS： The activated HSCs were divided into three groups： control gro...

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Published in:World journal of gastroenterology : WJG 2005-08, Vol.11 (30), p.4735-4739
Main Authors: Guo, Yan-Tong, Leng, Xi-Sheng, Li, Tao, Peng, Ji-Run, Song, Sheng-Han, Xiong, Liang-Fa, Qin, Zhi-Zhong
Format: Article
Language:English
Subjects:
Actins - metabolism
Animals
Apoptosis - drug effects
Base Sequence
Brief Reports
Cell Proliferation - drug effects
Collagen - metabolism
DNA - genetics
Hepatocytes - cytology
Hepatocytes - drug effects
Hepatocytes - metabolism
In Vitro Techniques
Ligands
PPAR gamma - agonists
PPAR gamma - genetics
PPAR gamma - metabolism
Rats
Rosiglitazone
Thiazolidinediones - pharmacology
生物学特性
细胞增殖
肝星形细胞
过氧物酶体
配合基
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Summary:AIM： To study the effect of rosiglitazone, which is a ligand of peroxisome proliferator-activated receptor gamma （PPARy）, on the expression of PPARy in hepatic stellate cells （HSCs） and on the biological characteristics of HSCs. METHODS： The activated HSCs were divided into three groups： control group, 3 μmol/L rosiglitazone group, and 10 μmol/L rosiglitazone group. The expression of PPARγ, α-smooth muscle actin （α-SMA）, and type Ⅰ and Ⅲ collagen was detected by RT-PCR, Western blot and immunocytochemical staining, respectively. Cell proliferation was determined with methylthiazolyltetrazolium （MTT） colodmetric assay. Cell apoptosis was demonstrated with flow cytometry. RESULTS： The expression of PPARγ at mRNA and protein level markedly increased in HSCs of 10 μmol/L rosiglitazone group （tvalue was 10.870 and 4.627 respectively, P〈0.01 in both）. The proliferation of HSCs in 10 μmol/L rosiglitazone group decreased significantly （t = 5.542, P〈0.01）, α-SMA expression level and type Ⅰ collagen synthesis ability were also reduced VS controls （tvalue = 10.256 and 14.627 respectively, P〈0.01 in both）. The apoptotic rate of HSCs significantly increased in 10 μmol/L rosiglitazone group vs control （X^2= 16.682, P〈0.01）. CONCLUSION： By increasing expression of PPARγ in activated HSCs, rosiglitazone, an agonist of PPARγ, decreases α-SNA expression and type Ⅰ collagen synthesis, inhibits cell proliferation, and induces cell apoptosis.
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v11.i30.4735