摘要
【目的】研究麦冬多糖对3T3-L1细胞诱导分化的脂肪细胞胰岛素敏感性作用机制的研究。【方法】将实验分为5组:模型对照组、阳性对照罗格列酮组、麦冬多糖低、中、高剂量组。体外诱导分化3T3-L1细胞为脂肪细胞,ELISA法检测各实验组3T3-L1脂肪细胞上清液中肿瘤坏死因子-α的表达量;RT-PCR法检测各实验组3T3-L1脂肪细胞瘦素、脂联素、抵抗素mRNA的表达水平。【结果】与模型对照组相比:其他实验组肿瘤坏死因子-α表达量降低,且3T3-L1脂肪细胞肿瘤坏死因子-α表达量随着麦冬多糖剂量的增加而降低;瘦素、脂联素mRNA表达升高,且3T3-L1脂肪细胞瘦素、脂联素mRNA表达随着麦冬多糖剂量的增加而增高;抵抗素mRNA的表达量随着麦冬多糖剂量的增加而降低。【结论】麦冬多糖降糖作用的部分机制可能与促进脂肪细胞高表达瘦素、脂联素而抑制TNF-α、抵抗素的表达而增加胰岛素的敏感性有关。
【Objective】To explore the mechanism of insulin sensibility of ophiopogonpolysaccharide in adipocytes induced from 3T3-L1 cells.【Methods】Experiment were divided into five groups: model control group, positive control rosiglitazone group, OPSR low,medium and high dose group. The 3T3-L1 cells were induced and differentiated into adipocytes in vitro. Concentrations of TNF-α in the supernatant were detected by ELISA and the mRNA expression levels of leptin, adiponectin and resistin in each group detected by RT-PCR.【Results】Compared with modle control group, the levels of TNF-αin other four groups were lower than the control, and the levels of TNF-α expression were decreased with the increase of OPSR dose than the control. The mRNA expression levels of leptin and adiponectin were higher than the control, and the levels increased while the dose of OPSR increased, but the result of resistin was opposite.【Conclusion】 The mechanism of lowering blood sugar of OPSR is partly associated with upregulation of the mRNA expression levels of leptin, adiponectin and downregulation of resistin and TNF-α to develop the sensibility of insulin.
出处
《武警后勤学院学报(医学版)》
CAS
2013年第1期5-8,共4页
Journal of Logistics University of PAP(Medical Sciences)
基金
武警后勤学院面上项目(WYM201017)
关键词
麦冬多糖
2型糖尿病
胰岛素抵抗
脂肪细胞
Ophiopogonpolysaccharide
Type 2 diabetes
Insulin resistance
Adipocyte