Curcumin blunt epithelial to mesenchymal transduction of hepatocytes to aggravate liver fibrosis through promoting autophagy in hepatocytes
10.3969/j.issn.1001-1978.2019.10.012
- Author:
De-Song KONG
1
Author Information
1. Scientific Research Dept, Nanjing Hospital of Chinese Medicine, Nanjing University of Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Autophagy;
Curcumin;
Epithelial-mesenchymal transition;
Hepatocyte;
Liver fibrosis;
Myofibroblast
- From:
Chinese Pharmacological Bulletin
2019;35(10):1388-1393
- CountryChina
- Language:Chinese
-
Abstract:
Aim To clarify the role of autophagy in the regulation mechanism of epithelial-mesenchymal transition(EMT) in hepatocytes and the transition to myofibroblast. Methods BNL CL. 2, a mouse embryonic hepatocyte, and BNL CL. 2 cells knocked-down BECN1 genes were treated with TGF-β1(2 μg . L-1) and curcumin(10, 20, 30 jimol • L - 1 ) . Real-time PCR and Western blot were used to detect Beclin-1, LC3, Vimentin and α-SMA gene and protein expression in BNL cl. 2 cells. The optical microscope was used to observe the changes of cell morphology. And the changes in cell autophagy were detected by GFPLC3 plasmid transfection. Results After the intervention of TGF-β1, the expression of Vimentin and α-SMA, the mesenchymal marker, increased and the autophagy decreased. Curcumin could inhibit Vimentin and a-SMA expression in hepatocytes. Moreover, curcumin could increase the autophagy related genes and protein expression of Beclin-1 and LC3 in hepatocytes. Curcumin could increase the level of autophagy and inhibit the cell transformation to myofibroblast-like cells. After interfering with BECN1, the effect of curcumin inhibiting hepatic EMT was partially blocked. Conclusions Curcumin could inhibit the process of EMT of hepatocytes by increasing the level of autophagy. The occurrence and development of liver fibrosis was consequently inhibited.
