Effects of Emodin against Renal Tubular Epithelial Cell Fibrosis via the Inhibition of Akt/mTOR Signal Pathway
- VernacularTitle:大黄素抑制Akt/mTOR通路抗肾小管上皮细胞纤维化的作用研究
- Author:
Fang DOU
1
;
Yi DING
;
Jianjie CHU
;
Weiwei LI
;
Wei ZHANG
;
Zeqiong NING
;
Xian ZHAO
;
Jingwen WANG
;
Aidong WEN
Author Information
1. 空军军医大学西京医院药剂科 西安710032
- Keywords:
Emodin;
Fibrosis;
Human renal tubular epithelial cell;
Akt/mTOR;
Autophagy
- From:
China Pharmacist
2018;21(10):1707-1711
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the mechanism of emodin ( EM) in the expression of related protein for the fibrosis of the transforming growth factor-β1(TGF-β1)-stimulated human renal tubular epithelial (HK-2) cells. Methods: HK-2 cells were randomly divided into the normal control group, TGF-β1-stimulated model control group and emodin ( TGF-β1 +EM) group. The contents of Collage Ⅰ and fibronectin in the culture supernatant were determined by ELISA. After HK-2 cells were stimulated with TGF-β1 for 24 h, the cells were collected for immunofluorescence, Western blot and RT-PCR analysis. RT-PCR was used to detect PI3K, p-Akt and mTOR. The protein expressions of PI3K, p-Akt and mTOR were detected by Western blot. Immunofluorescence was used to detect PI3K. Results: Compared with those in the model control group, the contents of CollageⅠand fibronectin in the supernatant of emod-in group significantly decreased (P<0. 05), the expression of PI3K protein was inhibited, the expression of downstream p-Akt protein decreased, and the downstream mTOR decreased (P<0. 05), the expression levels of PI3K, p-Akt and mTOR mRNA decreased, the differences were statistically significant (P<0. 05), and the expression of PI3K decreased. Conclusion: Emodin can alleviate fibrosis of HK-2 cells stimulated by TGF-β1 through the classical Akt/mTOR pathway of autophagy.
