中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (21): 3972-3974.doi: 10.3969/j.issn.1673-8225.2011.21.041

• 生物材料基础实验 basic experiments of biomaterials • 上一篇    下一篇

过氧化物酶体增殖物激活受体γ激动剂对二氧化硅致成纤维细胞纤维连接蛋白表达的影响

杜海燕   

  1. 齐鲁石化医院集团中心医院检验科，山东省淄博市  255400
  • 收稿日期:2010-10-13 修回日期:2010-12-10 出版日期:2011-05-21 发布日期:2011-05-21
  • 作者简介:杜海燕★，女，1977年生，山东省淄博市人，汉族，硕士，主管检验医师，主要从事临床细胞学研究。

Effects of peroxisome proliferator-activated receptor gamma agonists on fibronectin expression after SiO2 stimulation

Du Hai-yan   

  1. Department of Clinical Laboratory, Central Hospital of Qilu Petrochemical Hospital Group, Zibo 255400, Shandong Province, China
  • Received:2010-10-13 Revised:2010-12-10 Online:2011-05-21 Published:2011-05-21
  • About author:Du Hai-yan★, Master, Technician-in-charge, Department of Clinical Laboratory, Central Hospital of Qilu Petrochemical Hospital Group, Zibo 255400, Shandong Province, China duhaiyan007@163.com

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摘要：

背景: 过氧化物酶体增殖物激活受体γ激动剂对转化生长因子β1致矽肺肺间质纤维化作用的影响及机制尚不明确，罕见报道。
目的：观察过氧化物酶体增殖物激活受体γ激动剂对转化生长因子β1致矽肺肺纤维化作用的影响。
方法：200 mg/L SiO2刺激SD大鼠肺泡巨噬细胞培养上清液作用于中国仓鼠肺成纤维细胞株(CHL)建立矽肺纤维化的体外细胞模型。RT-PCR检测过氧化物酶体增殖物激活受体γ配体15d-PGJ2及其激动剂曲格列酮和齐格列酮对转化生长因子β1诱导CHL的纤维连接蛋白mRNA表达的影响。利用Western印迹技术观察过氧化物酶体增殖物激活受体γ激动剂对转化生长因子β1诱导CHL的纤维连接蛋白表达的影响。
结果与结论：①转化生长因子β1 mRNA表达呈一定范围内的剂量(0~5 μg/L)和时间(0~24 h)依赖效应。②过氧化物酶体增殖物激活受体γ配体及激动剂降低了纤维连接蛋白mRNA和蛋白的表达。结果提示过氧化物酶体增殖物激活受体γ激动剂可以抑制转化生长因子β1诱导的SiO2致肺成纤维细胞纤维连接蛋白合成，具有抗SiO2所致肺间质纤维化的潜在作用。

关键词: 矽肺, 过氧化物酶体类, 转化生长因子&beta, 纤维连接蛋白, 组织工程

Abstract:

BACKGROUND: The effect and mechanism of peroxisome proliferator-activated receptor gamma (PPARγ) agonists on transforming growth factor (TGF)-β1-induced fibrotic responses in lung fibroblasts remain unclear, and seldom reported.
OBJECTIVE: To study the effects of PPARγ agonists on TGF-β1-induced fibrotic responses in lung fibroblasts, so as to investigate its effects in preventing pulmonary interstitial fibrosis of silicosis.
METHODS: The pulmonary alveolar macrophage was prepared with 200 mg/L SiO2 and the supernatants were got. Chinese hamster lung fibroblasts were incubated with the prepared supernatants. Then a cellular model in vitro for studying pulmonary fibrosis induced by SiO2 was developed. Chinese hamster lung fibroblasts were cultured to observe the effects of the PPARγ ligand (15 d-PGJ2) and its agonists (troglitazone and ciglitazone) on the expression of TGF-β1-induced fibronectin. RT-PCR was used to detect the mRNA expression of fibronectin and Western blotting was used to detect the protein expression of fibronectin.
RESULTS AND CONCLUSION: (1) The expression of TGF-β1 mRNA showed an effect in a dose- (0-5 μg/L) and time-(0-24 hours) dependent manner. (2) PPARγ ligands and agonists reduced the mRNA and protein expressions of fibronectin. Results suggested that PPARγ agonists can inhibit TGF-β1-induced fibronectin synthesis after stimulation by SiO2 and may play a potential role in preventing pulmonary interstitial fibrosis.

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