随着酒精消费的增加,越来越多的人患有酒精性肝病(ALD)。因此,有必要从酒精代谢和危害方面阐述ALD的发病机制。在这项研究中,用不同浓度的乙醇和乙醛诱导L02细胞体外建立酒精性肝损伤模型。结果表明,乙醇的代谢可以促进ROS的含量,MDA,TNF-α,IL-6和caspase3,引起氧化和炎症应激和膜通透性变化。然而,未代谢的乙醇和乙醛对细胞膜通透性和炎症的影响很小,说明乙醇代谢产物是细胞膜损伤的主要原因。我们还评估了氨基酸(牛磺酸和蛋氨酸)的作用,维生素(E和维生素D),有机酸(苹果酸和柠檬酸),黄酮类化合物(芦丁和槲皮素),和酚酸(阿魏酸和绿原酸)对乙醇诱导的L02细胞的细胞膜损伤。绿原酸,牛磺酸,维生素E,柠檬酸对细胞膜损伤有显著的改善作用。苹果酸,芦丁,槲皮素,阿魏酸有明显的治疗作用,而维生素D和蛋氨酸的治疗效果较差。活性成分的结构与作用之间的关系可以进一步研究,以揭示其作用机理。和单体可以结合起来,探索功能成分之间是否存在协同作用,为实际的肝脏保护研究提供一定的理论依据。
With the increase in alcohol consumption, more and more people are suffering from alcoholic liver disease (ALD). Therefore, it is necessary to elaborate the pathogenesis of ALD from the aspects of alcohol metabolism and harm. In this study, we established an alcoholic liver injury model in vitro by inducing L02 cells with different concentration of ethanol and acetaldehyde. Results showed that the metabolism of ethanol can promote the content of ROS, MDA, TNF-α, IL-6, and caspase 3, causing oxidative and inflammatory stress and membrane permeability changes. However, unmetabolized ethanol and acetaldehyde had little effect on cell membrane permeability and inflammation, indicating that ethanol metabolites were the main reason for cell membrane damage. We also evaluated the effects of amino acids (taurine and methionine), vitamins (E and vitamin D), organic acids (malic acid and citric acid), flavonoids (rutin and quercetin), and phenolic acids (ferulic acid and chlorogenic acid) on alcohol-induced cell membrane damage of L02 cells. Chlorogenic acid, taurine, vitamin E, and citric acid had remarkable effects on improving cell membrane damage. Malic acid, rutin, quercetin, and ferulic acid had obvious therapeutic effects, while vitamin D and methionine had poor therapeutic effects. The relationship between the structure and effect of active ingredients can be further studied to reveal the mechanism of action, and monomers can be combined to explore whether there is a synergistic effect between functional components, in order to provide a certain theoretical basis for the actual study of liver protection.