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作 者:关蛟 张正筠[1] 周尊强[1] 佟大年[1] 周光文[1]
机构地区:[1]上海交通大学附属第六人民医院普外科,上海200233
出 处:《现代生物医学进展》2016年第14期2604-2607,共4页Progress in Modern Biomedicine
基 金:国家自然科学基金面上项目(81170721);上海市科委医学引导项目(14411960700);上海市科委浦江人才项目(14PJ1407300)
摘 要:目的:研究滤泡辅助性T细胞(Follicular Helper T cell,Tfh)在非肥胖性糖尿病小鼠(Non-obese Diabetic mice,NOD)发病过程中的作用机制。方法:实验动物NOD小鼠按血糖值分为胰岛炎组(血糖浓度≤9 mmol/L)及糖尿病组(血糖浓度≥20 mmol/L)。ELISA法检测各组中糖尿病自身抗体谷氨酸脱羧酶抗体(65-kda glutamate decarboxylase antibody,GAD65Ab)、抗胰岛素自身抗体(Insulin autoantibody,IAA)表达水平,Western blot检测B细胞型淋巴瘤6蛋白(B-cell lymphoma 6 protein,Bcl-6)及可诱导共刺激分子(Inducible costimulatory molecule,ICOS)表达,流式细胞仪检测各组外周血及脾脏Tfh细胞水平。结果:糖尿病组NOD鼠自身抗体GAD65Ab(1.21±0.23 nmol/L)、IAA(0.96±0.12 nmol/L)浓度较胰岛炎组(0.32±0.09 nmol/L,0.25±0.06 nmol/L)均有明显升高;糖尿病组NOD鼠Bcl-6及ICOS表达较胰岛炎组NOD鼠有明显升高,外周血和脾脏Tfh细胞水平糖尿病组NOD鼠(24.55%)较胰岛炎组NOD鼠(4.27%)升高明显。结论:NOD小鼠自发糖尿病与自身抗体浓度升高相关,Tfh细胞可能参与NOD鼠糖尿病发生及发展过程。Objective: To research the function mechanism of Follicular Helper T cell (Tfh) in Non-obese Diabetic mice (NOD). Methods: The NOD mice were divided into two groups according to their blood glucose level (Glu): the insulitis group (Glu≤ 9 mmol/L) and the diabetic group (Glu≥ 20 mmol/L). ELISA was used to test the level of diabetes autoantibody 65-kda glutamate decarboxylase antibody (GAD65Ab) and Insulin autoantibody (IAA). B-cell lymphoma 6 protein (Bcl-6) and Inducible costimulatory molecule (ICOS) were tested by Western blot. Tfh cell count was tested by Fluorescence activated cell sorting (FACS). Results: The level of GAD65Ab and IAA were much higher in diabetic group than that in insulitis group; Bcl-6 and ICOS were higher expressed indiabetic group than that in insulitis group; Tfla cell count were much higher in diabetic group than that in insulitis group. Conclusions: The autoantibody contributed to the diabetes progression and Tfh cell may participate in the pathogenesis of diabetes in NOD mice.
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