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Kuo, Chan-Yen; Chiu, Valeria; Hsieh, Po-Chun; Huang, Chun-Yen; Huang, S. Joseph; Tzeng, I-Shiang; Tsai, Fu-Ming; Chen, Mao-Liang; Liu, Chien-Ting; Chen, Yi-Ru
Journal of pharmacological sciences, November 2020, 2020-11-00, 20201101, 2020-11-01, Letnik: 144, Številka: 3Journal Article
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.
