To Explore the Effect of Tangnaikang on Smads Signaling Pathway of Human Renal Tubular Epithelial HK-2 Cell Induced by TGF-

YANG Li-xia; SHU Chang; WU Li-li; SUN Wen; LIU Tong-hua

doi:10.13422/j.cnki.syfjx.2014200160

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To Explore the Effect of Tangnaikang on Smads Signaling Pathway of Human Renal Tubular Epithelial HK-2 Cell Induced by TGF-

更新时间：2024-01-04

- To Explore the Effect of Tangnaikang on Smads Signaling Pathway of Human Renal Tubular Epithelial HK-2 Cell Induced by TGF-
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 20, Issue 20, Pages: 160-163(2014)
- 作者机构：
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- DOI：10.13422/j.cnki.syfjx.2014200160
  CLC： R285.5
- Published：2014
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YANG Li-xia, SHU Chang, WU Li-li, et al. To Explore the Effect of Tangnaikang on Smads Signaling Pathway of Human Renal Tubular Epithelial HK-2 Cell Induced by TGF-[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(20): 160-163.
DOI：

YANG Li-xia, SHU Chang, WU Li-li, et al. To Explore the Effect of Tangnaikang on Smads Signaling Pathway of Human Renal Tubular Epithelial HK-2 Cell Induced by TGF-[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(20): 160-163. DOI： 10.13422/j.cnki.syfjx.2014200160.

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-β1 10 μg ·L-1）、空白血清对照组（TGF-β1 10 μg ·L-1+10%空白血清）、TNK高浓度组（TGF-β1 10 μg ·L-1 +20%糖耐康含药血清）、TNK中浓度组（TGF-β1 10 μg ·L-1+10%糖耐康含药血清）、TNK低浓度组（TGF-β1 10 μg ·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。

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-β1 group (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-2 cultured with TGF-β1 were much notable than the control

and significantly decreased in HK-2 cultured with TGF-β1 plus 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.

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