Protective effects of oyster protein hydrolysates on alcohol-induced liver disease (ALD) in mice: based on the mechanism of anti-oxidative metabolism

with higher reducing power and ferric reducing antioxidant power (FRAP), and those capacities could be maintained at a high level after simulated gastrointestinal digestion. Compared to the model mice, oral administration (4 weeks) of AOPH at 800 mg per kg body weight could lead to a decline in T-AOC, GSH-PX, and ADH in the liver. The hepatocellular lesions were effectively relieved and impaired liver tissue development was successfully inhibited. A total of 834 genes and 54 proteins showed differential expression in the AOPH group and the oxidative metabolic pathways of ethanol such as oxidative phosphorylation, glutathione metabolism, peroxisomes, the PPAR signaling pathway and drug metabolism-cytochrome P450 play a preeminent role in ALD according to the results of transcriptomics and proteomics. The beneficial effects of AOPH were available in the improvement of ALD. These results revealed that AOPH intervention ameliorated ALD by affecting oxidative metabolism and highlighting AOPH's potential application as a functional food.