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Alcoholic liver disease (ALD) is associated with significant morbidity and mortality globally. In this study, the soybean lecithin-gallic acid complex was synthesized, and its physicochemical properties were evaluated, which confirmed the complex formation. Compared with the free state of the drug, gallic acid exhibited significantly different physicochemical properties after it was complexed with soybean lecithin. To clarify the binding mode between two monomers, computational investigation was performed. From the computational data, we deduced the structure of the compound and predicted that it has a high affinity for human phosphatidylcholine transfer protein and exhibits strong pharmacological activities in vivo. The complex not only effectively ameliorated liver fibrosis, lipid peroxidation, and oxidative stress, but also reduced liver iron overload in a mouse ALD model induced by alcohol (p &lt; 0.05). Additionally, it regulated iron metabolism by inhibiting TfR1 expression (p &lt; 0.05) and promoting hepcidin expression (p &lt; 0.05). These results suggest that the soybean lecithin-gallic acid complex ameliorates hepatic damage and iron overload induced by alcohol and exert hepatoprotective effects.

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Computational and biological investigation of the soybean lecithin–gallic acid complex for ameliorating alcoholic liver disease in mice with iron overload