Syringin inhibits insulin resistance through the PI3K/AKT pathway.

Abstract

This study aims to investigate the effects of syringin on insulin resistance (IR) and its mechanisms using an IR model in HepG2 cells. IR was induced by 10⁴ mol L^-1 insulin for 24 h, followed by syringin treatment at various concentrations for 48 h. Levels of glucose, triglycerides, TNF-α, IL-6, and GRP78 were measured, and protein expression of IRS-1, p-IRS-1, PI3K, p-PI3K, AKT, p-AKT, FoxO1, and p-FoxO1 was analysed by Western blot. Compared with controls, the IR model showed significant increases in glucose, triglycerides, TNF-α, IL-6, GRP78, and decreases in p-IRS1/IRS1, p-PI3K/PI3K, and p-AKT/AKT, with increased p-FoxO1/FoxO1 (all p < 0.01). Syringin (50-200 μg mL^-1) significantly lowered glucose, triglycerides, TNF-α, IL-6, and GRP78, and reversed these signalling changes by upregulating p-IRS1/IRS1, p-PI3K/PI3K, p-AKT/AKT and downregulating p-FoxO1/FoxO1 (p < 0.05). Syringin effectively ameliorates insulin resistance in HepG2 cells, lowers glucose and triglycerides, and improves glucose-lipid metabolism, likely via the PI3K/AKT pathway.