Mechanism of Action of Capsaicin and Quercitrin in Regulating Lipid Metabolism in HepG2 Cells through EGFR/PI3K/Akt Signaling Pathway

The objective of this study was to investigate the molecular mechanism behind the regulatory effect of capsaicin combined with quercitrin on liver lipid metabolism. The effects of capsaicin alone or in combination with quercitrin on the survival rate of HepG2 cells with oleic acid-induced lipid accumulation were investigated. Oil red O staining was used to observe lipid accumulation in HepG2 cells. Meanwhile, the levels of total triglyceride (TG), total cholesterol (TC), highdensity lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and total bile acid (TBA) were determined. Moreover, the expression levels of epidermal growth factor receptor (EGFR), phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), farnesoid X receptor 1 (FXR1), cholesterol 7α-hydroxylase (CYP7A1) and fibroblast growth factor 19 (FGF19) were determined by Western blotting. The results showed that the proliferation rate of HepG2 cells in each treatment group was greater than 75%, demonstrating no significant cytotoxicity. The results of oil red O staining showed a reduction in lipid accumulation in both single and combined treatment groups. The application of capsaicin alone or combined with quercitrin reduced the contents of TG, TC and LDL-C, increased the contents of HDL-C and TBA, and up-regulated the protein expression levels of EGFR, PI3K, Akt, FXR1 and FGF19. In summary, capsaicin combined with quercitrin exerted a synergistic regulatory effect on lipid metabolism in HepG2 cells, with the most pronounced effect being observed at a 3:1 ratio.