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作 者:董维平[1] 丁晓颖[1] 彭永德[1] 程群[1] 王育璠[1] 王煜非[1]
机构地区:[1]上海交通大学附属第一人民医院内分泌科糖尿病研究室,200080
出 处:《中华内分泌代谢杂志》2009年第2期186-188,共3页Chinese Journal of Endocrinology and Metabolism
基 金:基金项目:上海市科委重点课题基金(064119517);上海市科委引导计划项目(74119638)
摘 要:目的探讨脂肪细胞对共培养体系中胰岛细胞炎症状态的影响,以及α-硫辛酸对抗胰岛细胞炎症反应的作用。方法以单纯胰岛细胞培养为对照组、胰岛细胞-脂肪细胞共培养为实验组、胰岛细胞-脂肪细胞共培养加α-硫辛酸为干预组。以胰岛素释放试验比较胰岛细胞的功能,采用实时荧光PCR和Western印迹法检测细胞内IκB激酶(IKK)β的mRNA和蛋白水平。结果实验组胰岛素释放试验的分泌指数明显低于对照组和干预组(1.0±0.1vs2.6±0.2和2.5±0.5,P〈0.01)。实时荧光PCR显示,实验组的IKKβmRNA水平明显高于对照组和干预组(4.62±0.60vs1.00±0.46和2.25±0.75,P〈0.01)。Western印迹亦显示实验组的IKKβ蛋白水平明显高于对照丑和干预组。结论共培养体系中,脂肪细胞能激活胰岛细胞炎症信号通路的关键蛋白IKKβ,导致胰岛细胞受损;α-硫辛酸可抑制IKKβ的表达,保护胰岛细胞的功能。Objective To investigate the effects of differentiated 3T3-L1 adipocytes on inflammation of rat islet cells, as well as the protective effect of α-lipoic acid on the inflammation in vitro. Methods Rat islet cells were divided into three groups: the control group, the experimental co-culture system group(cocultured with differentiated mature 3T3-L1 adipocytes) and the intervention group (cocultured with mature 3T3-L1 adipocytes containing 4μg/ml α-lipoic acid). Insulin releasing test was performed for estimating the function of islet cells in culture supernatant of different groups. At the same time, the expression level of IKKβ in islet cells was detected by western blot and reahime PCR. Results There was significant decrease of insulin stimulation index (SI) in experimental co-cuhure system group compared with the control group and intervention group ( 1.0±0. 1 vs 2. 6±0. 2, 2.5±0.5 respectively; P〈0.01 ), while, the mRNA (4. 62±0. 60 vs 1.00±0.46 and2.25±0. 75;P〈0.01)and protein expression of IKKβ were significantly increased in the experimental group as compared with the other two groups. Conclusions In the co-cuhure system of adipocytes/islet cells, impaired function of islet cells could be induced by IKKβ activation, IKKβ was a key molecule in inflammation signal pathway in islet cells and could be activated by 3T3-L1 adipoeytes. α-lipoic acid was able to reverse the impaired function of islet cells by suppressing IKKβ expression.
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