【摘要】 目的:探讨糖耐康(TNK)含药血清对转化生长因子-β1(TGF-β1)诱导的人肾小管上皮细胞(HK-2)转分化Smad信号通路的影响。方法:将HK-2细胞用含10%胎牛血清的DMEM/F12(1∶1)培养基培养;实验分为6组:空白对照组、单纯TGF-β1诱导组(TGF-β110μg·L-1)、空白血清对照组(TGF-β110μg·L-1+10%空白血清)、TNK高浓度组(TGF-β110μg·L-1+20%糖耐康含药血清)、TNK中浓度组(TGF-β110μg·L-1+10%糖耐康含药血清)、TNK低浓度组(TGF-β110μg·L-1+5%糖耐康含药血清)。药物干预24 h后,荧光定量PCR检测TGF-β1及其Ⅰ,Ⅱ受体(TβRI,TβRⅡ)的mRNA表达,Western blot检测Smad 2、Smad 3的蛋白表达。结果:HK-2细胞经TGF-β1诱导后,TβRⅠ,TβRⅡ的mRNA表达和Smad 2,Smad 3的蛋白表达显著上升,与空白对照组相比有显著性差异(P<0.05),但经TNK含药血清干预后,其表达逐步下降,与单纯TGF-β1诱导组及TGF-β1+空白血清对照组相比有显著性差异(P<0.05)。而空白血清无此作用。结论:TNK能够调控TGF-β1诱导的人肾小管上皮细胞转分化Smad信号通路,在一定程度上具有抑制肾间质纤维化的作用。更多还原

【Abstract】 Objective: To explore the effect of Tangnaikang( TNK) on the smads signaling pathway of human renal tubular epithelial cells( HK-2) induced by transforming growth factor-β1( TGF-β1). Method: The HK-2 cells were cultured by DMEM /F12( 1 ∶ 1) with 10% fetal bovine serum and divided into control group,TGF-β1group( TGF-β110 μg·L-1),rat serum control group( TGF-β110 μg·L-1+ 10% rat serum),TNK-containing rat serum therapy groups( TGF-β110 μg·L-1+ 20% TNK or + 10% TNK or + 5% TNK). After 24 h,the expression of transforming growth factor β receptor I( TβRI),transforming growth factor β receptor II( TβRII) mRNA were tested by fluorescence quantitatiye PCR assay,and the expression of Smad 2,Smad 3 protein by Western-blot assay. Result: The expression of TβRI,TβRII mRNA and Smad 2,Smad 3 protein of HK-2cultured with TGF-β1were much notable than the control,and significantly decreased in HK-2 cultured with TGF-β1plus TNK compared with only TGF-β1( P <0.05),but only rat serum had no such effect. Conclusion:TNK could regulate the smads signaling pathway of human renal tubular epithelial cells HK-2 induced by transforming growth factor-β1,and could prevent the development of renal fibrosis to a certain extent.更多还原