大麻酚
氧化应激
抗氧化剂
药理学
细胞凋亡
鹅膏
生物
肝损伤
DNA损伤
肝细胞
生物化学
化学
体外
医学
大麻
植物
DNA
精神科
作者
Haowei Wang,Genmeng Yang,Xiaoxing Zhang,Huijie Zhang,Yan Liu,Chan Wang,Lin Miao,Yi Li,Yizhen Huang,Hanxin Teng,Shangwen Wang,Hao Cheng,Xiaofeng Zeng
标识
DOI:10.1016/j.fct.2023.114196
摘要
α-Amanitin, the primary lethal toxin of Amanita, specifically targets the liver, causing oxidative stress, hepatocyte apoptosis, and irreversible liver damage. As little as 0.1 mg/kg of α-amanitin can be lethal for humans, and there is currently no effective antidote for α-amanitin poisoning. Cannabidiol is a non-psychoactive natural compound derived from Cannabis sativa that exhibits a wide range of anti-inflammatory, antioxidant, and anti-apoptotic effects. It may play a protective role in preventing liver damage induced by α-amanitin. To investigate the potential protective effects of cannabidiol on α-amanitin-induced hepatocyte apoptosis and oxidative stress, we established α-amanitin exposure models using C57BL/6J mice and L-02 cells in vitro. Our results showed that α-amanitin exposure led to oxidative stress, apoptosis, and DNA damage in both mouse hepatocytes and L-02 cells, resulting in the death of mice. We also found that cannabidiol upregulated the level of Nrf2 and antioxidant enzymes, alleviating apoptosis, and oxidative stress in mouse hepatocytes and L-02 cells and increasing the survival rate of mice. Our findings suggest that cannabidiol has hepatoprotective effects through the regulation of Nrf2 and antioxidant enzymes and may be a potential therapeutic drug for Amanita poisoning.
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