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。
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.
出处
《现代生物医学进展》
CAS
2013年第7期1210-1213,共4页
Progress in Modern Biomedicine
基金
国家自然科学基金项目(81102128)
