Abstract:This study employed a mouse model of alcoholic liver injury for experiments, and combined network pharmacology to explore the protective effect of safflower extract on alcoholic liver injury and its potential molecular mechanisms. A mouse model of alcoholic liver injury was established by intragastric administration of 50% absolute ethanol. The mice were intervened with different doses of safflower extract for 30 days. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) indicators, triglyceride (TG), total cholesterol (TC), and malondialdehyde (MDA), as well as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), were detected, and the results were verified by pathological sections of liver tissue. The results showed that safflower extract significantly reduced serum ALT and AST levels and inhibited the accumulation of triglyceride and total cholesterol in liver tissue of model mice. It effectively reduced the content of malondialdehyde and increased the activities of superoxide dismutase and glutathione peroxidase, and the high-dose group had the most significant effect. Network pharmacology analysis showed that the active components of safflower (such as quercetin and kaempferol) acted on the core targets such as AKT1, JUN, TP53, and were significantly enriched in the PI3K-Akt, MAPK, and AGE-RAGE signaling pathways. Studies have shown that safflower extract can play an anti-oxidation, anti-inflammation and regulation of lipid metabolism by regulating the above signaling pathways, thereby reducing alcohol-induced hepatocyte injury.