Institute of Biochemistry and Cell Biology, IBBC-CNR, Rome, Italy.
Department of Ecological and Biological Sciences, University of Tuscia, Viterbo, Italy.
Nutrition. 2020 Nov-Dec;79-80:110783. doi: 10.1016/j.nut.2020.110783. Epub 2020 Mar 2.
Uncontrolled ingestion of alcohol has dramatic consequences on the entire organism that are also associated with the oxidation process induced by alcohol and elevate radical oxygen species. Resveratrol, a nonflavonoid phenol, shows well-documented antioxidant properties. We investigated the potential antioxidant ability of this natural compound in a mouse model of alcohol addiction.
We administered (per os) for 60 d 10 mg · kg · d of resveratrol in alcoholic adult male mice. Oxidative stress was evaluated by measuring serum-free oxygen radicals defense and free oxygen radical levels. Resveratrol metabolites were measured in the serum of mice that were administered with resveratrol. Finally, the effect of resveratrol on the alcohol-induced alteration of brain-derived neurotrophic factors (BDNF) in the liver was investigated.
Prolonged consumption of resveratrol strongly counteracts serum radical oxygen species formation caused by chronic alcohol intake without effects on natural, free oxygen radical defense. The presence of resveratrol metabolites in the serum only of animals supplemented with resveratrol potentiates the evidence that the antioxidant effect observed is due to the ingestion of the natural compound. Moreover, resveratrol supplementation can counteract alcohol-induced BDNF elevation in the liver, which is the main target of organ alcohol-induced damage.
The consumption of resveratrol through metabolite formation may play a protective role by decreasing free radical formation and modulating the BDNF involved in hepatic disruption induced by chronic alcohol consumption. Further investigation into the mechanism underlying the protective effect could reinforce the potential use of resveratrol as a dietary supplement to prevent damage associated with chronic alcohol abuse.
酒精的不受控制的摄入对整个机体产生巨大影响，这与酒精诱导的氧化过程以及升高的自由基有关。白藜芦醇是一种非类黄酮酚，具有良好的抗氧化特性。我们在酒精成瘾的小鼠模型中研究了这种天然化合物的潜在抗氧化能力。
我们通过口服给予 60 天，每天 10 毫克/千克的白藜芦醇给成年雄性酒精摄入的小鼠。通过测量血清游离氧自由基防御和游离氧自由基水平来评估氧化应激。在给予白藜芦醇的小鼠的血清中测量白藜芦醇代谢物。最后，研究了白藜芦醇对酒精诱导的肝源性神经营养因子（BDNF）改变的影响。
长期摄入白藜芦醇强烈抵消了慢性酒精摄入引起的血清自由基形成，而对天然的游离氧自由基防御没有影响。只有在补充白藜芦醇的动物的血清中存在白藜芦醇代谢物，这增强了观察到的抗氧化作用是由于摄入天然化合物的证据。此外，白藜芦醇补充可以抵消酒精诱导的肝 BDNF 升高，肝是酒精诱导损伤的主要靶器官。
通过代谢物形成摄入白藜芦醇可能通过减少自由基形成和调节与慢性酒精摄入引起的肝破坏有关的 BDNF 发挥保护作用。对保护作用机制的进一步研究可以增强白藜芦醇作为膳食补充剂预防与慢性酒精滥用相关的损伤的潜在用途。
