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. 2020 Nov;144(3):172-182.
doi: 10.1016/j.jphs.2020.07.014. Epub 2020 Aug 6.

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

Chan-Yen Kuo  1 , Valeria Chiu  2 , Po-Chun Hsieh  3 , Chun-Yen Huang  4 , S Joseph Huang  5 , I-Shiang Tzeng  6 , Fu-Ming Tsai  7 , Mao-Liang Chen  8 , Chien-Ting Liu  9 , Yi-Ru Chen  10
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Free article

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

Chan-Yen Kuo et al. J Pharmacol Sci. 2020 Nov.
Free article

Abstract

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.

Keywords: Chrysophanol; ER stress; Ferroptosis; Hepatic stellate cells; Lipid reactive oxygen species.

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Conflict of interest statement

Declaration of competing interest The authors declare no conflicts of interest. The funders played no role in the study design, data collection, analysis, and interpretation, the writing of the manuscript, or the decision to publish the results.

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