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Emodin-induced autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes

Authors Zheng X, Yang S, Zhang R, Wang S, Li G, Zhou S

Received 12 February 2019

Accepted for publication 5 July 2019

Published 3 September 2019 Volume 2019:13 Pages 3171—3180


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Tuo Deng

Xiao-yuan Zheng1, Shi-ming Yang2, Rong Zhang1, Su-min Wang2, Guo-bing Li1, Shi-wen Zhou1

1Department of Pharmacy, Xinqiao Hospital, Army Medical University, Chongqing, People’s Republic of China; 2Department of Gastroenterology, Xinqiao Hospital, Army Medical University, Chongqing, People’s Republic of China

Correspondence: Shi-wen Zhou
Department of Pharmacy, Xinqiao Hospital, Army Medical University, Chongqing 400037, People’s Republic of China

Background: Emodin, a major component of Polygonum multiflorum (PM), has been reported to exert both protective and toxic effects in several cell types. However, the effects and underlying mechanisms of action of emodin in hepatic cells are still obscure.
Methods: The present study used the normal human liver cell line L02 to investigate the effects and mechanisms of emodin in hepatic cells. After treatment with emodin, L02 cells were examined for viability, apoptosis and autophagy with the Cell Counting Kit-8 (CCK-8), annexin V/PerCP staining and GFP-LC3 plasmid transfection. The expression of proteins including cleaved caspase-3, LC3B-I/II, p-PI3K, PI3K, p-AKT, AKT, p-mTOR, mTOR and actin was examined by using Western blot.
Results: Emodin significantly inhibited the viability of and induced apoptosis in L02 cells in a dose- and time-dependent manner. In addition, emodin increased the number of GFP-LC3 puncta in L02 cells and upregulated the expression of LC3B-II compared to those in control cells. Furthermore, emodin significantly decreased the expression of p-PI3K, p-AKT and p-mTOR in a dose-dependent manner compared to that in control cells without altering the expression of PI3K, AKT and mTOR. Notably, cotreatment with emodin and 3-methyladenine (3-MA) or rapamycin significantly increased and decreased the apoptosis rate of L02 cells, respectively, compared to that of cells treated with emodin alone.
Conclusion: In conclusion, emodin exhibited cytotoxicity in the L02 human hepatic cell line by promoting apoptosis, and it also induced autophagy through the suppression of the PI3K/AKT/mTOR signalling pathway. The autophagy could play a protective role following emodin treatment.

Keywords: Polygonum multiflorum, emodin, hepatoprotective, apoptosis, hepatotoxic, autophagy, PI3K, AKT, mTOR

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