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

被引:16
作者
Guo, Yan-Tong [1 ]
Leng, Xi-Sheng [1 ]
Li, Tao [1 ]
Peng, Ji-Run [1 ]
Song, Sheng-Han [1 ]
Xiong, Liang-Fa [1 ]
Qin, Zhi-Zhong [1 ]
机构
[1] Peking Univ Peoples Hosp, Dept Gen Surg, Beijing 100044, Peoples R China
基金
中国国家自然科学基金;
关键词
Peroxisome proliferator-activated receptor gamma; Hepatic stellate cell; Rosiglitazone;
D O I
10.3748/wjg.v11.i30.4735
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
AIM: To study the effect of rosiglitazone, which is a ligand of peroxisome proliferator-activated receptor gamma (PPAR gamma), on the expression of PPAR gamma in hepatic stellate cells (HSCs) and on the biological characteristics of HSCs. METHODS: The activated HSCs were divided into three groups: control group, 3 mu mol/L rosiglitazone group, and 10 mu mol/L rosiglitazone group. The expression of PPAR gamma, alpha-smooth muscle actin (alpha-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) colorimetric assay. Cell apoptosis was demonstrated with flow cytometry. RESULTS: The expression of PPAR gamma at mRNA and protein level markedly increased in HSCs of 10 mu mol/L rosiglitazone group (t value was 10.870 and 4.627 respectively, P<0.01 in both). The proliferation of HSCs in 10 mu mol/L rosiglitazone group decreased significantly (t = 5.542, P<0.01), alpha-SMA expression level and type I collagen synthesis ability were also reduced vs controls (t value = 10.256 and 14.627 respectively, P<0.01 in both). The apoptotic rate of HSCs significantly increased in 10 mu mol/L rosiglitazone group vs control (chi(2) = 16.682, P<0.01). CONCLUSION: By increasing expression of PPAR gamma in activated HSCs, rosiglitazone, an agonist of PPAR gamma, decreases alpha-SMA expression and type I collagen synthesis, inhibits cell proliferation, and induces cell apoptosis. (C) 2005 The WJG Press and Elsevier Inc. All rights reserved.
引用
收藏
页码:4735 / 4739
页数:5
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