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

Abstract

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.