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目的:研究S型雌马酚(S-Equol,S-Eq)对高糖培养HepG2人肝癌细胞株胰岛素敏感性和胰岛素受体底物(insulin receptor substrate,IRS)-1表达的影响并探讨其可能的分子机制。方法:高糖培养HepG2细胞,1、10、100μM S-Eq处理细胞后,MTT法检测细胞活力,硫酸蒽酮比色法检测胰岛素刺激细胞糖原合成量,Realtime PCR和Western blot法分别检测IRS-1 mRNA及蛋白表达变化。结果:S-Eq对HepG2细胞活力无明显影响,但显著改善高糖培养条件下HepG2细胞胰岛素敏感性,其中10μM S-Eq+H组胰岛素刺激后细胞糖原合成量上升最为显著(P<0.01),同时发现,S-Eq能显著上调IRS-1 mRNA和蛋白表达量。结论:S-Eq可能通过调控IRS-1的表达,增强高糖培养HepG2细胞胰岛素敏感性,这可能是S-Eq发挥其抗糖尿病作用的重要理论依据。
Objective: To investigate the effect of S-Equol (S-Eq) on insulin sensitivity and insulin receptor substrate (IRS) -1 expression in HepG2 human hepatocellular carcinoma cell line with high glucose Possible molecular mechanisms. Methods: HepG2 cells were cultured in high glucose and cells were treated with 1, 10, 100 μM S-Eq. MTT assay was used to detect cell viability. Sulfuric acid anthrone colorimetric assay was used to detect insulin-stimulated cellular glycogen synthesis. Realtime PCR and Western blot were used to detect IRS -1 mRNA and protein expression changes. Results: S-Eq had no significant effect on the viability of HepG2 cells, but significantly improved the insulin sensitivity of HepG2 cells under high glucose conditions. The amount of glycogen synthesis increased most significantly after stimulated with insulin (10μM S-Eq + H group) (P <0.01 ), And found that S-Eq can significantly up-regulate IRS-1 mRNA and protein expression. CONCLUSIONS: S-Eq may enhance the insulin sensitivity of HepG2 cells cultured in high glucose by regulating the expression of IRS-1, which may be an important theoretical basis for S-Eq to exert its anti-diabetic effect.