Panax notoginseng Saponins Alleviate TGF-β1-induced Renal Tubular Epithelial Cell Injury by Inhibiting Autophagy
10.13422/j.cnki.syfjx.20221304
- VernacularTitle:三七皂苷通过抑制自噬减轻TGF-β1诱导的肾小管上皮细胞损伤
- Author:
Wen MAO
1
;
Linying XIA
1
;
Xianli LIU
1
;
Liping PAN
2
;
Yueguang DU
1
Author Information
1. School of Basic Medicine，Zhejiang Chinese Medical University，Hangzhou 310053，China
2. School of Life Sciences，Zhejiang Chinese Medical University，Hangzhou 310053，China
- Publication Type:Journal Article
- Keywords:
Panax notoginseng saponins;
renal tubular epithelial cells;
transforming growth factor-β1 （TGF-β1）;
autophagy
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(20):86-91
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the role and mechanism of Panax notoginseng saponins （PNS） in inhibiting transforming growth factor-β1 （TGF-β1）-induced renal tubular epithelial cell injury. MethodNRK-52E renal tubular epithelial cells were cultured and divided into control group， TGF-β1 group，TGF-β1+12.5 mg·L-1 PNS group，TGF-β1+25 mg·L-1 PNS group and TGF-β1+50 mg·L-1 PNS group. After 48 hours of PNS intervention， the cells and the supernatant were collected， and cell morphology was observed by inverted microscope. Western blot was used to detect the expression of epithelial-mesenchymal transition （EMT）-related proteins and autophagy-related proteins. Flow liquid chromatography for multiple protein quantification and flow cytometry were employed to determine the content of inflammatory factors and apoptosis rate， respectively. ResultCompared with the conditions in the control group， after TGF-β1 induction， the cells showed a spindle-shaped change and the expression of E-cadherin was down-regulated （P<0.05）， while the expression of α-smooth muscle actin （α-SMA） was up-regulated （P<0.05）. After PNS treatment， most of the cells tended to be normal and reversed the occurrence of EMT. In addition， compared with the conditions in the control group， the level of TNF-α was increased while that of IL-10 was decreased， with elevated apoptosis rate （P<0.05） in the TGF-β1 group. After PNS treatment， the level of TNF-α was lowered while that of IL-10 was boosted with the increase of the dose， with reduced apoptosis rate （P<0.05）. Moreover， after TGF-β1 induction， the expression of autophagy-related proteins Beclin 1 and LC3Ⅱ/Ⅰ in renal tubular epithelial cells were up-regulated， while PNS inhibited their expression（P<0.05，P<0.01）. ConclusionPNS had a protective effect on TGF-β1-induced renal tubular epithelial cells， and the mechanism might be that it reduced inflammation and apoptosis by inhibiting autophagy， thus alleviating TGF-β1-induced injury.
