Sulforaphane Alleviates α-Amanitin-Induced Liver Injury by Modulating Pink1-Parkin Pathway
- 1Department of Clinical Veterinary Medicine, College of Veterinary Medicine, , Jin Hei Road No. 95, Panlong District, Kunming 650051, China
- 2Yunnan Plateau Characteristic Agricultural Industry Research Institute, , Kunming 650201, China
- 3Faculty of Veterinary Medicine, , Khon Kaen 40002, Thailand
Abstract
Background: α-Amanitin (α-AMA) is the primary lethal toxin found in poisonous mushrooms of the genus Amanita; accidental ingestion can lead to severe liver injury, and there is currently no specific antidote. Due to its significant anti-inflammatory and antioxidant activity, Sulforaphane (SFN) has attracted increasing attention for its role in preventing liver injury. However, it remains unclear whether SFN can alleviate α-AMA-induced liver injury. This study aimed to elucidate the protective effects of SFN against α-AMA-induced liver injury and its potential molecular mechanisms. Methods and Results: The results showed that SFN significantly reduced serum ALT and AST levels in α-AMA-intoxicated mice (p < 0.01), alleviated pathological damage such as hepatic edema, lobular rupture, and inflammatory infiltration, reduced apoptosis, lowered MDA levels, and simultaneously increased CAT activity (p < 0.01). In AML-12 cells, SFN effectively reversed α-AMA-induced cellular damage (including reduced cell viability and decreased mitochondrial membrane potential). This study further found that SFN significantly upregulated the expression of Pink1 and Parkin. Furthermore, the overexpression of Pink1 significantly alleviated α-AMA-induced oxidative stress, mitochondrial damage, and apoptosis. Conclusions: The above results indicate that SFN may alleviate α-AMA-induced liver damage by promoting the expression of Pink1 and Parkin, improving mitochondrial dysfunction, and inhibiting apoptosis.
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BibTeX
@article{sun2026sulforaphane,
title = {{Sulforaphane Alleviates α-Amanitin-Induced Liver Injury by Modulating Pink1-Parkin Pathway}},
author = {Jian Sun and Yangyang Li and Zehui Li and Zhijie Liu and Zhengwang Yi and Peng Wu and Juyu Wang and Weijie Qu and Bundit Tengjaroenkul and Yi Wu and Xiaolong Gu},
journal = {Nutrients},
year = {2026},
month = oct,
doi = {10.3390/nu18193282},
url = {https://europepmc.org/article/PMC/PMC13666618},
note = {CC BY},
}
RIS
TY - JOUR
TI - Sulforaphane Alleviates α-Amanitin-Induced Liver Injury by Modulating Pink1-Parkin Pathway
AU - Jian Sun
AU - Yangyang Li
AU - Zehui Li
AU - Zhijie Liu
AU - Zhengwang Yi
AU - Peng Wu
AU - Juyu Wang
AU - Weijie Qu
AU - Bundit Tengjaroenkul
AU - Yi Wu
AU - Xiaolong Gu
PY - 2026
DA - 2026/10/01
JO - Nutrients
DO - 10.3390/nu18193282
UR - https://europepmc.org/article/PMC/PMC13666618
AB - Background: α-Amanitin (α-AMA) is the primary lethal toxin found in poisonous mushrooms of the genus Amanita; accidental ingestion can lead to severe liver injury, and there is currently no specific antidote. Due to its significant anti-inflammatory and antioxidant activity, Sulforaphane (SFN) has attracted increasing attention for its role in preventing liver injury. However, it remains unclear whether SFN can alleviate α-AMA-induced liver injury. This study aimed to elucidate the protective effects of SFN against α-AMA-induced liver injury and its potential molecular mechanisms. Methods and Results: The results showed that SFN significantly reduced serum ALT and AST levels in α-AMA-intoxicated mice (p < 0.01), alleviated pathological damage such as hepatic edema, lobular rupture, and inflammatory infiltration, reduced apoptosis, lowered MDA levels, and simultaneously increased CAT activity (p < 0.01). In AML-12 cells, SFN effectively reversed α-AMA-induced cellular damage (including reduced cell viability and decreased mitochondrial membrane potential). This study further found that SFN significantly upregulated the expression of Pink1 and Parkin. Furthermore, the overexpression of Pink1 significantly alleviated α-AMA-induced oxidative stress, mitochondrial damage, and apoptosis. Conclusions: The above results indicate that SFN may alleviate α-AMA-induced liver damage by promoting the expression of Pink1 and Parkin, improving mitochondrial dysfunction, and inhibiting apoptosis.
SN - 2072-6643
ER -