2009•Chinese Journal of Integrated Traditional and Western NephrologyRequires access

Study on Effect of Astragali on ECM Excretion in Renal Tubular Epithelial Cells Induced by TGF-β_1 and its Possible Mechanism

Youmin Peng

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Abstract

Objective:To investigate the effects of astragali on the ECM excretion in renal tubular epithelial cells induced by TGF-β1 and its possible mechanism.Methods:Human renal tubular epithelial (HK-2) cells were divided into four groups as follows:control group,TGF-β1 group(TGF-β1 5 ng/ml),TGF-β1 5 ng/ml and astragali 100 μg/ml group,TGF-β1 5 ng/ml and astragali 1 mg/ml group.Fibronectin (FN) protein was detected by ELISA.Plasminogen activator inhibitor-1 ( PAI-1) protein was detected by Western blot.The mRNA of FN and PAI-1 were measured by RT-PCR.Results:(1)HK-2 cells expressed small amounts of FN and PAI-1.(2)The levels of PAI-1 and FN mRNA were significantly increased in HK-2 cells induced by TGF-β1 compared with those of control group (P0.01).PAI-1 and FN protein were significantly raised in HK-2 cells stimulated by TGF-β1 compared with those of control group (P0.01).(3)Astragali could inhibit PAI-1 and FN mRNA and protein expression compared with TGF-β1 group (P0.01),especially 1 mg/ml astragali.Conclusion:Astragali could inhibit the expressions of PAI-1 and FN in human renal tubular epithelial cell induced by TGF-β1,which may be one of the mechanisms contributing to retardation of the progression of the renal tubulointerstitial fibrosis.

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Objective:To investigate the effects of astragali on the ECM excretion in renal tubular epithelial cells induced by TGF-β1 and its possible mechanism.Methods:Human renal tubular epithelial (HK-2) cells were divided into four groups as follows:control group,TGF-β1 group(TGF-β1 5 ng/ml),TGF-β1 5 ng/ml and astragali 100 μg/ml group,TGF-β1 5 ng/ml and astragali 1 mg/ml group.Fibronectin (FN) protein was detected by ELISA.Plasminogen activator inhibitor-1 ( PAI-1) protein was detected by Western blot.The mRNA of FN and PAI-1 were measured by RT-PCR.Results:(1)HK-2 cells expressed small amounts of FN and PAI-1.(2)The levels of PAI-1 and FN mRNA were significantly increased in HK-2 cells induced by TGF-β1 compared with those of control group (P0.01).PAI-1 and FN protein were significantly raised in HK-2 cells stimulated by TGF-β1 compared with those of control group (P0.01).(3)Astragali could inhibit PAI-1 and FN mRNA and protein expression compared with TGF-β1 group (P0.01),especially 1 mg/ml astragali.Conclusion:Astragali could inhibit the expressions of PAI-1 and FN in human renal tubular epithelial cell induced by TGF-β1,which may be one of the mechanisms contributing to retardation of the progression of the renal tubulointerstitial fibrosis.

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Available abstract

Objective:To investigate the effects of astragali on the ECM excretion in renal tubular epithelial cells induced by TGF-β1 and its possible mechanism.Methods:Human renal tubular epithelial (HK-2) cells were divided into four groups as follows:control group,TGF-β1 group(TGF-β1 5 ng/ml),TGF-β1 5 ng/ml and astragali 100 μg/ml group,TGF-β1 5 ng/ml and astragali 1 mg/ml group.Fibronectin (FN) protein was detected by ELISA.Plasminogen activator inhibitor-1 ( PAI-1) protein was detected by Western blot.The mRNA of FN and PAI-1 were measured by RT-PCR.Results:(1)HK-2 cells expressed small amounts of FN and PAI-1.(2)The levels of PAI-1 and FN mRNA were significantly increased in HK-2 cells induced by TGF-β1 compared with those of control group (P0.01).PAI-1 and FN protein were significantly raised in HK-2 cells stimulated by TGF-β1 compared with those of control group (P0.01).(3)Astragali could inhibit PAI-1 and FN mRNA and protein expression compared with TGF-β1 group (P0.01),especially 1 mg/ml astragali.Conclusion:Astragali could inhibit the expressions of PAI-1 and FN in human renal tubular epithelial cell induced by TGF-β1,which may be one of the mechanisms contributing to retardation of the progression of the renal tubulointerstitial fibrosis.

Key concepts: Fibronectin, Plasminogen activator, Western blot, Transforming growth factor, Messenger RNA, Plasminogen activator inhibitor-1, Internal medicine, Excretion

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