PPAR-γ在小鼠肺成纤维细胞中的抗纤维化作用

Antifibrotic effects of PPAR-γ in mouse lung fibroblasts

目的探讨过氧化物酶体增殖物激活受体-γ(PPAR-γ)在小鼠肺成纤维细胞中的抗纤维化作用及机制。方法体外培养小鼠肺成纤维细胞(C57BL/6),以转化生长因子-2(TGF-β2)刺激其转换为肌纤维母细胞,使用不同浓度PPAR-γ配体罗格列酮(RSG)抑制转化,采用细胞生长计数检测细胞增殖;PCR检测PPAR-γmRNA、血小板衍生生长因子-β(PDGFR-β)mRNA及成纤维细胞生长因子R1(FGF-R1)mRNA转录水平。结果 RSG抑制C57BL/6细胞增殖(P<0.05);PPAR-γmRNA转录水平随RSG浓度增加而表达增加,PDGF-βmRNA随RSG浓度增加而表达减少,FGF-R1mRNA转录水平与RSG无关(P>0.05)。结论 RSG抑制TGF-β2诱导的小鼠肺成纤维细胞生物学特性改变,其可能机制与使PPAR-γ活化及PDGF-β表达下调相关。

ObjectiveTo explore the role and mechanism of PPAR-γin inhibiting the fibrosis process of mouse lung fibroblasts.MethodsMouse lung fibroblasts from C57BL/6mice were cultured,stimulated for transformation with transforming growth factorβ2,and inhibited for transition by different concentrations of rosiglitazone(RSG).Cell proliferation was detected by cell counting,PCR was employed to examine transcriptional expression of PPAR-γ,platelet derived growth factorR-β(PDGFR-β),and fibroblast growth factor R1(FGFR1).ResultsRSG inhibited C57BL/6fibroblast proliferation(P<0.05).The relative levels of PPAR-γmRNA and PPAR-γprotein increased with the increasing concentration of RSG,and the expression of PDGFR-βmRNA decreased with the increasing concentration of RSG.The concentration alteration of RSG had nothing to do with the expression of FGFR1mRNA(P<0.05).ConclusionRSG can inhibit the induction of TGF-β2in alterations of biological characteristics of C57BL/6fibroblasts.Possibly,it activates the PPAR-γand downregulates the expression of PDGF-β.