中文摘要：

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。

英文摘要：

Objective： To investigate the effect of S-Equol on insulin sensibility and IRS-1 expression of HepG2 exposed to high glucose and the possible molecular mechanisms. Methods： HepG2 cells were cultured in high glucose in the absence or presence 1, 10, 100 μM S-Eq. Effect of S-Eq on viability of cells was detected by MTT assay. The insulin-stimulated glycogen content of cells was evaluated by anthrone-sulfuric colorimetry. The mRNA and protein expression levels of IRS-1 were estimated by Real-time PCR and Western blot analysis, respectively. Results： There was no significant influence on viability of HepG2 cells by S-Eq. But the insulin sensibility was significantly increased by S-Eq and insulin-stimulated glycogen content was up-regulated by S-Eq at the concentration of 100μM（P〉0.01）. We also found S-Eq significantly raised the levels of IRS-1 mRNA and protein. Conclusion： S-Eq can effectively improve insulin sensi- bility of HepG2 cells exposed to high glucose by regulating IRS-1 and this may be the critical theoretical basis of anti-diabetic effect of S-Eq.