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Gandouling ameliorates liver injury in Wilson's disease through the inhibition of ferroptosis by regulating the HSF1/HSPB1 pathway.

Authors :
Zhao, Chenling
Chen, Jie
Tian, Liwei
Wen, Yuya
Wu, Mingcai
Tang, Lulu
Zhou, An
Xie, Wenting
Dong, Ting
Source :
Journal of Cellular & Molecular Medicine; Sep2024, Vol. 28 Issue 17, p1-13, 13p
Publication Year :
2024

Abstract

Ferroptosis, an iron‐dependent form of cell death, plays a crucial role in the progression of liver injury in Wilson's disease (WD). Gandouling (GDL) has emerged as a potential therapeutic agent for preventing and treating liver injury in WD. However, the precise mechanisms by which GDL mitigates ferroptosis in WD liver injury remain unclear. In this study, we discovered that treating Toxic Milk (TX) mice with GDL effectively decreased liver copper content, corrected iron homeostasis imbalances, and lowered lipid peroxidation levels, thereby preventing ferroptosis and improving liver injury. Bioinformatics analysis and machine learning algorithms identified Hspb1 as a pivotal regulator of ferroptosis. GDL treatment significantly upregulated the expression of HSPB1 and its upstream regulatory factor HSF1, thereby activating the HSF1/HSPB1 pathway. Importantly, inhibition of this pathway by NXP800 reversed the protective effects of GDL on ferroptosis in the liver of TX mice. In conclusion, GDL shows promise in alleviating liver injury in WD by inhibiting ferroptosis through modulation of the HSF1/HSPB1 pathway, suggesting its potential as a novel therapeutic agent for treating liver ferroptosis in WD. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15821838
Volume :
28
Issue :
17
Database :
Complementary Index
Journal :
Journal of Cellular & Molecular Medicine
Publication Type :
Academic Journal
Accession number :
179639297
Full Text :
https://doi.org/10.1111/jcmm.70018