Chrysophanol attenuates hepatitis B virus X protein-induced hepatic stellate cell fibrosis by regulating endoplasmic reticulum stress and ferroptosis

Chrysophanol attenuates hepatitis B virus X protein-induced hepatic stellate cell fibrosis by regulating endoplasmic reticulum stress and ferroptosis

Hepatitis B virus X protein (HBx) and hepatic stellate cells (HSCs) are critical for liver fibrosis development. Anti-fibrosis occurs via reversion to quiescent-type HSCs or clearance of HSCs via apoptosis or ferroptosis. We aimed to elucidate the role of chrysophanol in rat HSC-T6 cells expressing...

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Bibliographic Details
Main Authors: Chan-Yen Kuo, Valeria Chiu, Po-Chun Hsieh, Chun-Yen Huang, S. Joseph Huang, I-Shiang Tzeng, Fu-Ming Tsai, Mao-Liang Chen, Chien-Ting Liu, Yi-Ru Chen
Format: Article
Language:English
Published: Elsevier 2020-11-01
Series:Journal of Pharmacological Sciences
Subjects:
Hepatic stellate cells
Chrysophanol
Lipid reactive oxygen species
ER stress
Ferroptosis
Online Access:http://www.sciencedirect.com/science/article/pii/S1347861320300797
Description
Summary:Hepatitis B virus X protein (HBx) and hepatic stellate cells (HSCs) are critical for liver fibrosis development. Anti-fibrosis occurs via reversion to quiescent-type HSCs or clearance of HSCs via apoptosis or ferroptosis. We aimed to elucidate the role of chrysophanol in rat HSC-T6 cells expressing HBx and investigate whether chrysophanol (isolated from Rheum palmatum rhizomes) influences cell death via ferroptosis in vitro. Analysis of lipid reactive oxygen species (ROS), Bip, CHOP, p-IRE1α, GPX4, SLC7A11, α-SMA, and CTGF showed that chrysophanol attenuated HBx-repressed cell death. Chrysophanol can impair HBx-induced activation of HSCs via endoplasmic reticulum stress (ER stress) and ferroptosis-dependent and GPX4-independent pathways.
ISSN:1347-8613

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