Thonningianin A ameliorates acetaminophen-induced liver injury by activating GPX4 and modulating endoplasmic reticulum stress

TA treatment significantly lowered plasma ALT and AST levels, inhibited the production of inflammatory cytokines, and reduced oxidative stress markers in liver tissues. Furthermore, TA modulated apoptosis-related proteins by increasing BCL-2 expression while decreasing CHOP and BAX levels. It alleviated endoplasmic reticulum (ER) stress by downregulating GRP78, p-PERK, and ATF4. Notably, liver-specific GPX4 knockdown, achieved through AAV-8-mediated shRNA delivery, abolished the hepatoprotective effects of TA, underscoring GPX4's essential role in mediating TA-induced hepatoprotection. These findings suggest TA as a promising therapeutic agent in managing APAP-induced liver injury, with its unique action on both oxidative and ER stress pathways contributing to its hepatoprotective efficacy.

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Publication Details

Journal
Frontiers in Pharmacology
Published
2025-02-20
DOI
https://doi.org/10.3389/fphar.2025.1531277
Citations
5
Primary Topic
Drug-Induced Hepatotoxicity and Protection
Type
article
Field-Weighted Citation Impact
7.79

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article

Thonningianin A ameliorates acetaminophen-induced liver injury by activating GPX4 and modulating endoplasmic reticulum stress

Xiangyou Hu, Yingyan Ye, Shanglei Lai, Xiaobing Dou et al.
5 citations
Frontiers in Pharmacology
Drug-Induced Hepatotoxicity and Protection
7.79
article

Thonningianin A ameliorates acetaminophen-induced liver injury by activating GPX4 and modulating endoplasmic reticulum stress

Xiangyou Hu, Yingyan Ye, Shanglei Lai, Xiaobing Dou, Ai Fu, Qinchao Ding, Wenjing Cao, Qingsheng Liu, Lan Wu, Xuchen Qi
article en
5 citations

Abstract

TA treatment significantly lowered plasma ALT and AST levels, inhibited the production of inflammatory cytokines, and reduced oxidative stress markers in liver tissues. Furthermore, TA modulated apoptosis-related proteins by increasing BCL-2 expression while decreasing CHOP and BAX levels. It alleviated endoplasmic reticulum (ER) stress by downregulating GRP78, p-PERK, and ATF4. Notably, liver-specific GPX4 knockdown, achieved through AAV-8-mediated shRNA delivery, abolished the hepatoprotective effects of TA, underscoring GPX4's essential role in mediating TA-induced hepatoprotection. These findings suggest TA as a promising therapeutic agent in managing APAP-induced liver injury, with its unique action on both oxidative and ER stress pathways contributing to its hepatoprotective efficacy.

Frontiers in PharmacologyVol. 16
Zhejiang Chinese Medical University (CN), Sir Run Run Shaw Hospital (CN), Hangzhou Hospital of Traditional Chinese Medicine (CN), Hangzhou Xixi hospital (CN), Shaoxing People's Hospital (CN), Hangzhou Medical College (CN), Zhejiang University (CN)
National Natural Science Foundation of China, China Postdoctoral Science Foundation
Openalex Percentile: Top 3%
Drug-Induced Hepatotoxicity and Protection
7.79
DOIOpen Access PDFOpenAlex
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Thonningianin A ameliorates acetaminophen-induced liver injury by activating GPX4 and modulating endoplasmic reticulum stress — Xiangyou Hu, Yingyan Ye, et al. · Frontiers in Pharmacology (2025) | TGRS Research Map | TGRS