2. Academic Validation
  3. Cannabidiol protects the liver from α-Amanitin-induced apoptosis and oxidative stress through the regulation of Nrf2

Cannabidiol protects the liver from α-Amanitin-induced apoptosis and oxidative stress through the regulation of Nrf2

  • Food Chem Toxicol. 2023 Dec:182:114196. doi: 10.1016/j.fct.2023.114196.
Haowei Wang 1,  Genmeng Yang 1,  Xiaoxing Zhang 1,  Huijie Zhang 1,  Yan Liu 1,  Chan Wang 1,  Lin Miao 1,  Yi Li 1,  Yizhen Huang 1,  Hanxin Teng 2,  Shangwen Wang 3,  Hao Cheng 4,  Xiaofeng Zeng 5
Affiliations

Affiliations

  • 1 NHC Key Laboratory of Drug Addiction Medicine, Department of Forensic Medicine, School of Forensic Medicine, Kunming Medical University, Kunming, China.
  • 2 Department of Pathogen Biology and Immunology, School of Basic Medical Science, Kunming Medical University, Kunming, China.
  • 3 NHC Key Laboratory of Drug Addiction Medicine, Department of Forensic Medicine, School of Forensic Medicine, Kunming Medical University, Kunming, China. Electronic address: [email protected].
  • 4 NHC Key Laboratory of Drug Addiction Medicine, Department of Forensic Medicine, School of Forensic Medicine, Kunming Medical University, Kunming, China. Electronic address: [email protected].
  • 5 NHC Key Laboratory of Drug Addiction Medicine, Department of Forensic Medicine, School of Forensic Medicine, Kunming Medical University, Kunming, China. Electronic address: [email protected].
PMID: 37992955 DOI: 10.1016/j.fct.2023.114196
Abstract

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.

Keywords

Apoptosis; Cannabidiol; Hepatocytes; Nuclear factor erythroid 2–related factor 2 (Nrf2); α-Amanitin.

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