Protective effects of astragalosides Ⅳ on renal proximal tubular epithelial cell injury induced by high glucose
10.3760/cma.j.issn.1008-1372.2018.11.008
- VernacularTitle:黄芪甲苷对高糖诱导的肾小管上皮细胞损伤的保护作用及机制研究
- Author:
Yaning WANG
1
;
Yunfang ZHANG
;
Yunqi LIU
;
Jinxiang GAO
Author Information
1. 256603,山东省滨州医学院附属医院肾内科
- Keywords:
Astragalus membranaceus;
Saponins/PD;
Kidney tubules;
Epithelial cells/DE;
Diabetic nephropathies;
Rats
- From:
Journal of Chinese Physician
2018;20(11):1632-1636
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effects of astragalosides Ⅳ (ASI) on high glucose-induced renal proximal tubular epithelial cells (NRK-52E).Methods NRK-52E were cultured and divided randomly into three groups:control group,high glucose group (HG in short),ASI groups (with various doses).Cells were treated with increasing concentrations of ASI (20,40,80 and 100 μg/ml) for 24 h in high glucose and we also stimulated cells in ASI 100 μg/ml with high glucose for various lengths of time.The apoptosis rate was detected by flow cytometric analysis.The mRNA and protein expression of transforming growth factor-β1 (TGF-β1),a-smooth muscle actin (α-SMA),Smad2,Smad3 and their phosphorylated forms were detected by real-time polymerase chain reaction (PCR) and Western blot,respectively.Results Compared with the control group,apoptosis was increased in the high glucose group (P ＜ 0.01).However,ASI inhibited high glucose-induced cell apoptosis in a dose-dependent manner,with a maximal inhibitory effect achieved at 100 μg/ml (P ＜ 0.05).The significant inhibition caused by ASI was observed at 8h after the start of pretreatment (P ＜ 0.05) and increased in a time-dependent manner.ASI can inhibit the expression of TGF-β1,α-SMA,Smad2,Smad3 both at mRNA and protein level.Conclusions ASI inhibited NRK-52E cells apoptosis induced by high glucose and reduced expression of TGF-β1,α-SMA,Smad2,Smad3 both at the mRNA and protein level in NRK-52E cells,thus delayed epithelial-to-mesenchymal transition progress.
