首页> 中文期刊> 《中国药理学通报 》 >全反式维甲酸对HFL-Ⅰ细胞α-平滑肌肌动蛋白、Ⅰ型胶原、热休克蛋白47表达的影响

全反式维甲酸对HFL-Ⅰ细胞α-平滑肌肌动蛋白、Ⅰ型胶原、热休克蛋白47表达的影响

             

摘要

目的 研究全反式维甲酸(ATRA)对转化生长因子-β1(TGF-β1)诱导的人胚肺成纤维细胞(HFL-Ⅰ)中α-平滑肌肌动蛋白(α-SMA),Ⅰ型胶原(Collagen-Ⅰ),热休克蛋白47(HSP47) mRNA和蛋白表达的影响.方法 体外培养HFL-Ⅰ细胞,MTT法检测不同浓度TGF-β1和ATRA分别作用3 d对HFL-Ⅰ细胞增殖能力的影响.随后分为6组:对照组、5 μg·L-1 TGF-β1组、10 μmol·L-1 ATRA组、5 μg·L-1 TGF-β1+0.1 μmol·L-1 ATRA组、5 μg·L-1 TGF-β1+1 μmol·L-1 ATRA组、5 μg·L-1 TGF-β1+10 μmol·L-1 ATRA组,RT-PCR和Western blot方法分别检测各实验组细胞中α-SMA,Collagen-Ⅰ,HSP47 mRNA和蛋白的表达.结果 ① MTT法检测结果显示不同浓度的TGF-β1可刺激HFL-Ⅰ细胞增殖,呈浓度依赖性(P<0.05);不同浓度的ATRA对HFL-Ⅰ细胞增殖能力均有明显抑制作用,并随药物浓度的增加而增强(P<0.05).② 5 μg·L-1 TGF-β1诱导后,HFL-Ⅰ细胞中α-SMA,Collagen-I,HSP47 mRNA和蛋白表达均明显上调(P<0.05).③ ATRA以浓度依赖性方式下调经TGF-β1诱导的HFL-Ⅰ细胞中α-SMA,Collagen-I,HSP47 mRNA和蛋白的表达(P<0.05).结论 ATRA能够抑制TGF-β1诱导的HFL-Ⅰ细胞的分化,其作用机制可能与降低Collagen-I、HSP47表达有关.%Aim To investigate the effects of all-transretinoic acid ( ATRA ) on the expression of α-smooth muscle actin( α-SMA ), Collagen-Ⅰ and heat shock protein 47 ( HSP47 ) in the TCF-β1-stimulated human lung fibroblasts ( HFL- Ⅰ ). Methods Firstly, cell proliferation of HFL- Ⅰ was detected by MTT after the cells were treated with different concentrations of TGF β1 and ATRA respectively for 3 days. HFL- Ⅰ cells in vitro were divided into six experimental groups: the control group; 5 μg · L-1 TGF-β1 group; 10 μmol · L-1 ATRA group; 5 μg · L-1 TGF-β1 +0. 1 μmol · L-1 ATRA group; 5 μg · L-1 TCF-β1 +1 μmol · L-1 ATRA group; 5 μg · L-1 TGF-β1 + lOμmol · L-1 ATRA group. Expressions of α-SMA, Collagen- Ⅰ HSP47 were determined through RT-PCR and Western blot. Results Different concentrations of TGF-β1 and ATRA could respectively promote cell proliferation of HFL- Ⅰ in a concentration-dependent manner. Furthermore. in a concentration-dependent manner. ATRA reduced the mRNA and protein expressions of α-SMA. Collagen- Ⅰ and HSP47 which obviously increased in the TGF-β1-stimulated HFL- Ⅰ cells. Conclusions ATRA can inhibit TGF-β1-stimulated differentiation and proliferation of HFL- Ⅰ cells. The mechamsm may be related to the down-regulation of the expression of Collagen- Ⅰ and HSP47.

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