DOI: https://doi.org/10.2478/acph-260022
Article ID: 260022 (15 pages)
Article
Syringin inhibits insulin resistance through the PI3K/AKT pathway
Abstract
Abstract:
Objective: To investigate the effects of syringin on insulin resistance (IR) and its mechanisms using an IR model in HepG2 cells.
Methods: IR was induced by 10^-4 mol/L 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 analyzed by western blot.
Results: 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, p-AKT/AKT, with increased p-FoxO1/FoxO1 (all P < 0.01). Syringin (50–200 μg/mL) significantly lowered glucose, triglycerides, TNF-α, IL-6, and GRP78, and reversed these signaling changes by upregulating p-IRS1/IRS1, p-PI3K/PI3K, p-AKT/AKT and downregulating p-FoxO1/FoxO1 (P < 0.05).
Conclusion: Syringin effectively ameliorates insulin resistance in HepG2 cells, lowers glucose and triglycerides, and improves glucose-lipid metabolism, likely via the PI3K/AKT pathway.
Keywords
Keywords: syringin, insulin resistance, PI3K, AKT, HepG2
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