Cannabidiol protects liver from binge alcohol-induced steatosis by mechanisms including inhibition of oxidative stress and increase in autophagy |
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| Institution: | 1. Department of Medicine, National Taiwan University Hospital Hsin-Chu Branch, Hsin-Chu City, Taiwan;2. School of Medicine, National Taiwan University, Taipei City, Taiwan;3. Department of Medical Laboratory Science and Biotechnology, Yuanpei University, Hsin-Chu City, Taiwan;4. Department of Laboratory Medicine, Taipei Hospital, Ministry of Health and Welfare, New Taipei City, Taiwan;5. Institute of Biotechnology, National Taiwan University, Taipei, Taiwan;6. Division of Infectious Diseases, Department of Internal Medicine, Changhua City, Taiwan;7. Center for Infectious Diseases Research, Changhua Christian Hospital, Changhua City, Taiwan;8. Department of Nursing, College of Medicine & Nursing, Hung Kuang University, Taichung, Taiwan;2. Department of Biochemistry and Molecular Biology, Federal University of Parana, Campus Centro Politecnico, CP 19046, 81531-980 Curitiba, PR, Brazil |
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| Abstract: | Acute alcohol drinking induces steatosis, and effective prevention of steatosis can protect liver from progressive damage caused by alcohol. Increased oxidative stress has been reported as one mechanism underlying alcohol-induced steatosis. We evaluated whether cannabidiol, which has been reported to function as an antioxidant, can protect the liver from alcohol-generated oxidative stress-induced steatosis. Cannabidiol can prevent acute alcohol-induced liver steatosis in mice, possibly by preventing the increase in oxidative stress and the activation of the JNK MAPK pathway. Cannabidiol per se can increase autophagy both in CYP2E1-expressing HepG2 cells and in mouse liver. Importantly, cannabidiol can prevent the decrease in autophagy induced by alcohol. In conclusion, these results show that cannabidiol protects mouse liver from acute alcohol-induced steatosis through multiple mechanisms including attenuation of alcohol-mediated oxidative stress, prevention of JNK MAPK activation, and increasing autophagy. |
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| Keywords: | Alcohol Steatosis Cannabidiol Oxidative stress Autophagy Free radicals |
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