Abstract
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.
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