Abstract / Summary
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.