【摘要】 目的采用转化生长因子-β1(transforming growth factor-β1,TGF-β1)在体外刺激大鼠肾系膜细胞表达纤维连接蛋白(fibronectin),观察全反式维甲酸(all-trans retinoicacid,atRA)对它的作用及对TGF-β1的Smad通路的影响。方法用Western blot方法检测TGF-β1诱导的肾系膜细胞纤维连接蛋白表达,Smad2的磷酸化,磷酸化Smad2、总Smad2/3和Smad4的核转位,以及atRA对TGF-β1的这些作用的影响。结果atRA能抑制TGF-β1诱导的肾系膜细胞纤维连接蛋白表达。atRA对TGF-β1引起的Smad2的磷酸化无明显作用,但atRA能部分阻断TGF-β1引起的磷酸化Smad2、Smad2/3和Smad4核转位。结论atRA体外拮抗TGF-β1的致纤维化效应可能是由其减少磷酸化Smad2、Smad2/3、Smad4的核转位所致。更多还原

【Abstract】 Purpose To investigate the effects of all-trans retinoic acid （atRA） on transforming growth factor-β1 （TGF-β1）-induced fibronectin expression and Smad pathway activation in cultured rat renal mesangial cells. Methods Fibronectin expression, phosphorylation of Smad 2, nuclear translocation of phospho-Smad 2, total Smad 2/3, Smad 4 induced by TGF-β1 in the presence or absence of atRA in the mesangial cells were analysed by Western blotting. Results atRA inhibited fibronectin expression induced by TGF-β1. atRA did not affect TGF-β1-induced phosphorylation of Smad 2, however, atRA attenuated TGF-β1-induced nuclear translocation of phospho-Smad 2, Smad 2/3, and Smad 4. Conclusions The in vitro anti-fibrotic actions of atRA are presumably due to a decreased nuclear translocation of phospho-Smad 2, Smad 2/3 and Smad 4 in mesangial cells stimulated with TGF-β₁.更多还原