2013Zhongguo zhongyiyao xinxi zazhiRequires access

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

Fan Li

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Abstract

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 cells were cultured by DMEM/F12(1∶1) with 10% fetal bovine serum and divided into control group,TGF-β1 group(TGF-β110 ng/mL),blank serum control group(TGF-β110 ng/mL + 10% animal serum),TNK drug-containing serum therapy groups(TGF-β110 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-β1group(P 0.05),but blank serum control group had no such effect.Conclution TNK could prevent the development of renal fibrosis to some extent through regulating the expression of Smads signaling pathway.

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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 cells were cultured by DMEM/F12(1∶1) with 10% fetal bovine serum and divided into control group,TGF-β1 group(TGF-β110 ng/mL),blank serum control group(TGF-β110 ng/mL + 10% animal serum),TNK drug-containing serum therapy groups(TGF-β110 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-β1group(P 0.05),but blank serum control group had no such effect.Conclution TNK could prevent the development of renal fibrosis to some extent through regulating the expression of Smads signaling pathway.

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Available abstract

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 cells were cultured by DMEM/F12(1∶1) with 10% fetal bovine serum and divided into control group,TGF-β1 group(TGF-β110 ng/mL),blank serum control group(TGF-β110 ng/mL + 10% animal serum),TNK drug-containing serum therapy groups(TGF-β110 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-β1group(P 0.05),but blank serum control group had no such effect.Conclution TNK could prevent the development of renal fibrosis to some extent through regulating the expression of Smads signaling pathway.

Key concepts: SMAD, Transforming growth factor, Messenger RNA, Internal medicine, Endocrinology, Receptor, Chemistry, Medicine

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Effect of Tangnaikang on Expression of Smad 2,3,7mRNA of Human Renal Tubular Epithelial Cell HK-2 Induced by TGF-β_1 — Research Paper | ScholarLens