文献类型：期刊文献

中文题名：糖耐康对转化生长因子-β_1诱导人肾小管上皮细胞Smad 2、3、7mRNA表达的影响

英文题名：Effect of Tangnaikang on Expression of Smad 2,3,7mRNA of Human Renal Tubular Epithelial Cell HK-2 Induced by TGF-β_1

作者：李芳[1];杨丽霞[2];舒畅[1];刘铜华[3];吴丽丽[3];孙文[3]

第一作者：李芳

机构：[1]甘肃中医学院;[2]甘肃省中医药研究院;[3]北京中医药大学

第一机构：甘肃中医药大学

年份：2013

卷号：20

期号：11

起止页码：37

中文期刊名：中国中医药信息杂志

外文期刊名：Chinese Journal of Information on Traditional Chinese Medicine

收录：CSTPCD;;CSCD:【CSCD_E2013_2014】；

基金：国家自然科学基金面上项目(30973909);北京中医药大学创新团队项目(2011-CXTD-19)

语种：中文

中文关键词：糖耐康;转化生长因子-β1;人肾小管上皮细胞;Smad;2基因;Smad;3基因;Smad;7基因

外文关键词：Tangnaikang; TGF-β1; human renal tubular epithelial cell; Smad 2 mRNA; Smad 3 mRNA;Smad 7 mRNA

摘要：目的观察糖耐康药物血清干预转化生长因子-β1(TGF-β1)诱导的人肾小管上皮细胞(HK-2)Smad 2、3、7 mRNA的表达,探讨其在防治肾间质纤维化方面的作用。方法将HK-2细胞用含10%胎牛血清的DMEM/F12(1∶1)培养基培养;实验分为空白对照组、单纯TGF-β1诱导组(TGF-β110 ng/mL)、空白血清对照组(TGF-β110 ng/mL+10%空白血清)、干预1组(TGF-β110 ng/mL+5%糖耐康药物血清)、干预2组(TGF-β110 ng/mL+10%糖耐康药物血清)、干预3组(TGF-β110 ng/mL+20%糖耐康药物血清)。药物干预24 h后,荧光定量PCR检测Smad 2、3、7 mRNA的表达。结果 HK-2细胞经TGF-β1诱导后,Smad 2、3 mRNA的表达显著上升,而Smad 7的表达减弱,与空白对照组比较差异有统计学意义(P<0.05),经糖耐康药物血清干预后,Smad 2、3 mRNA的表达逐步下降,而Smad 7 mRNA的表达逐步上升,与单纯TGF-β1诱导组比较差异有统计学意义(P<0.05)。结论糖耐康在一定程度上能够抑制TGF-β1诱导的人肾小管上皮细胞纤维化,其机制可能与调节纤维化信号通路Smad 2、3、7mRNA表达有关。
Objective Through studying the effect of Tangnaikang （TNK） on the expression of Smad 2, 3, 7 mRNA of human renal tubular epithelial cells HK-2 induced by transforming growth factor-β1 （TGF-β1）, to explore the mechanism of TNK on prevention and treatment of renal fibrosis. Methods The HK-2 ceils were cultured by DMEM/F12 （1：1） with 10% fetal bovine serum and divided into control group, TGF-β1 group {TGF--β1 10 ng/mL）, blank serum control group （TGF-β1 10 ng/mL ＋ 10% animal serum）, TNK drug-containing serum therapy groups （TGF-β1 10 ng/mL ＋ 5% TNK or ＋ 10% TNK or ＋ 20% TNK）. After 24 h, the expression of Smad 2, 3, 7 mRNA were tested by fluorescence quantitatiye PCR assay. Results After the HK-2 cells were induced by TGF-β1, the expression of Smad 2, 3 mRNA were increased and the expression of Smad 7 mRNA was decreased compared with the control group （P〈0.05）. The expression of Smad 2, 3 mRNA were decreased and the expression of Smad 7 mRNA was increased in TNK drug-containing serum therapy groups compared with TGF-β1 group （P〈0.05）, but blank serum control group had no such effect. Condution TNK could prevent the development of renal fibrosis to some extent through regulating the expression of Smads signaling pathway.