AcSDKP对TGF-β1诱导大鼠MSCs向肌成纤维细胞分化的抑制作用  

Inhibitory Effect of AcSDKP on the Myofibroblast Differentiation of Rat Mesenchymal Stem Cells Induced by Transforming Growth Factor-β1 in vitro

作　　者：唐文岘[1] 张月娟[1] 张君[1] 熊蕾[1] 汪保和[1] 

机构地区：[1]湖南师范大学生命科学学院,湖南长沙410081

出　　处：《激光生物学报》2016年第2期142-146,184,共6页Acta Laser Biology Sinica

基　　金：湖南省教育厅科学研究项目(12C0219);湖南省教育厅科研项目资助(15B099);湖南师范大学青年科学基金项目;中医诊断国家重点学科开放基金(2013ZYZD23);湖南中医药大学青年基金(99820001-100)

摘　　要：目的:研究N-乙酰基-丝氨酰-天冬氨酰-赖氨酰-脯氨酸(N-acetyl-seryl-aspartly-lysyl-proline,Ac SDKP)对转化生长因子β1(Transforming growth factor beta 1,TGF-β1)诱导大鼠骨髓间充质干细胞(mesenchymal stem cells,MSCs)向肌成纤维细胞(myofibroblast,MF)分化的影响,探讨Ac SDKP抗纤维化作用的可能机制。方法:全骨髓贴壁法分离培养大鼠骨髓MSCs。使用免疫组化,Western blotting技术分析α-SMA蛋白的表达以及Smad2/3,ERK1/2蛋白磷酸化的变化情况。结果:和对照组相比,TGF-β1诱导的MSC中α-SMA、磷酸化-Smad2/3及磷酸化-ERK1/2的表达大大增强,使用Ac SDKP干预细胞则三者的表达量明显下降且呈一定的剂量依赖性。结论:Ac SDKP可以显著抑制TGF-β1诱导的大鼠MSCs向MF分化,可能通过抑制TGF-β/Smad/ERK1/2信号通路的激活,从而发挥其抗器官纤维化作用。Objective: To investigate the effects of antifibrotic peptide N-acetyl- seryl-aspartly-lysyl-proline( Ac SDKP)on the differentiation of rat MSCs into myofibroblasts mediated by transforming growth factor beta- 1( TGF-β1). To explore the possible anti-fibrotic mechanisms of Ac SDKP in depth. Methods: Isolated the mesenchymal stem cells( MSCs) by the whole bone marrow culture method. The protein expressions of α-SMA and the changes of phosphoSmad2 /3 and phospho- ERK1 /2 were detected by immunocytochemistry and Western blotting. Results: Compared with the control group,the protein expressions of α-SMA,p-Smad2 /3,p-ERK1 /2 were greatly increased in MSCs which was induced by TGF-β1,and showed a dose-dependent decrease in Ac SDKP group. Conclusion: Ac SDKP markedly inhibit the differentiation of rat MSCs into myofibroblasts probably by blocking the TGF-β / Smad / ERK1 /2 signaling pathway activation,and thus mediating its anti fibrosis activity.

关 键 词：间充质干细胞 N-乙酰基丝氨酰天门冬酰赖氨酰脯氨酸 转化生长因子Β1 纤维化 

分 类 号：Q813.1[生物学—生物工程]