Mechanistic Study of Glycyrrhizic Acid Improving Alcoholic Fatty Liver Disease by Modulating the SHP1/SYK Signaling Pathway in Macrophages.

OBJECTIVE

To investigate glycyrrhizin's effects and molecular mechanisms on the progression of alcoholic fatty liver.

METHODS

An alcoholic fatty liver model was established, followed by the administration of glycyrrhizin ammonium (20 mg/kg). Liver tissue pathological changes were observed using oil red O staining, and pyroptotic bodies were observed using transmission electron microscopy. Western blot was used to detect the expression of related proteins. To establish a model of alcoholic fatty liver cells to explore the molecular mechanism of glycolic acid in this disease.

RESULTS

Glycyrrhizin ammonium reduced the area of oil red staining in liver tissue and the number of pyroptotic bodies decreased the relative protein expression of NOX2, NOX3, p-SYK, STING, p-PDE4B, NLRP3, IL-1β, GSDMD, Caspase-1, and Caspase-4, and increased the relative protein expression of p-SHP1 and Nrf2.

CONCLUSION

Glycyrrhizin ameliorates the progression of alcoholic fatty liver by modulating the SHP1/SYK signaling pathway in macrophages, thereby inhibiting hepatic lipid peroxidation and pyroptosis.