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榼藤子总皂苷改善胰岛素抵抗机制的初步研究 被引量:5

Mechanisms and Effect of Total Saponins from Entada phaseoloides on the Insulin Resistance
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摘要 目的:研究榼藤子总皂苷对2型糖尿病大鼠模型胰岛素敏感性的影响,利用HepG-2胰岛素抵抗细胞模型初步研究其可能的分子机制。方法:①通过高脂饲料喂养结合注射小剂量链脲佐菌素(STZ)建立II型糖尿病大鼠模型。实验大鼠随机分为正常对照组、模型组、阳性对照组(二甲双胍,200 mg.kg-1)、榼藤子总皂苷低、中、高剂量组(25,50,100 mg.kg-1)。待约4周模型成立后,各组ig给药观察榼藤子总皂苷对糖尿病模型大鼠胰岛素敏感性的影响。②用含0.25 mmol.L-1软脂酸和3%BSA的DMEM培养基刺激HepG-2细胞48 h建立胰岛素抵抗细胞模型,实验分正常组、模型组、阳性对照组(二甲双胍,2 mmol.L-1)、榼藤子总皂苷低、高质量浓度组(50,100 mg.L-1)。采用Western blot方法比较各种处理下蛋白酪氨酸磷酸酶-1B(PTP-1B)蛋白的表达水平。结果:2型糖尿病大鼠ITT数据显示,同模型组相比,榼藤子总皂苷各给药组的胰岛素敏感性均有所提高。在正常情况下,HepG-2细胞内PTP-1B的表达水平能被胰岛素下调;而在HepG-2细胞胰岛素抵抗模型细胞中,PTP-1B较正常组表达增加,且其表达水平不再受胰岛素调控,榼藤子总皂苷处理可以明显缓解这种状况。结论:榼藤子总皂苷能够改善2型糖尿病大鼠模型的胰岛素耐受,可能是通过影响PTP-1B的表达水平改善肝细胞胰岛素耐受。 Objective: To study the effect of total saponins from Entada phaseoloides (TSEP) on insulin resistance in type 2 diabetes rats and exploring the molecular mechanism using HepG-2 insulin resistance hepatocytes. Method: Type 2 diabetic rat model was established by high-fat diet and low-dose streptozotocin. Insulin tolerance test was performed to determine the effect of TSEP on insulin resistance. (~)Insuin resistance in HepG-2 cells was induced by 0.25 mmol ~ L-1 of palmitic acid. The expression levels of protein tyrosine phosphatase-lB (PTP-1B) among different treatment groups were compared by Western blot. Result: Compared with the model group, the insulin sensitivity in the TSEP treated rats was increased. In normal HepG-2 cells, the protein levels of PTP-1B were decreased after insulin treatment. However, its expression level could not be ameliorated by TSEP. Conclusion: TSEP can improve the insulin resistance in type 2 diabetes mellitus rats. A possible mechanism underlying the insulin resistanceby TSEP in hepatocytes may be related to modulating PTP-1B expression.
出处 《中国实验方剂学杂志》 CAS 北大核心 2012年第20期157-161,共5页 Chinese Journal of Experimental Traditional Medical Formulae
基金 国家自然科学基金项目(81073150)
关键词 榼藤子总皂苷 2型糖尿病 胰岛素抵抗 total saponins from Entada phaseoloides type 2 diabetes mellitus insulin resistance
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