Effects of Emodin against Renal Tubular Epithelial Cell Fibrosis via the Inhibition of Akt/mTOR Signal Pathway / 中国药师

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.