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首页> 外文期刊>Sports medicine - open >Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes
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Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes

机译:运动训练但未补充姜黄素可降低1型糖尿病遗传易感性模型胰岛中的免疫细胞浸润

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BackgroundThe main mechanism involved in the pathogenesis of autoimmunity is an uncontrolled inflammatory response against self-antigens. Therefore, anti-inflammatory factors, such as the intake of bioactive compounds and a physically active lifestyle, may decrease or cease the development of autoimmune diseases. Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic β cell destruction. The non-obese diabetic (NOD) mouse is a model of spontaneous T1D and is the model most similar to human disease. MethodsTo determine the effects of exercise training and curcumin supplementation on T1D progression, 48 NOD mice, 5?weeks old, were randomly divided into four groups: control, curcumin supplementation, trained, and trained plus curcumin. Every 2?weeks, blood glucose was measured using a glucometer. At the end of 20?weeks, a histopathological procedure was used to assess immune cells infiltration into pancreatic β cells (insulitis). ResultsModerate intensity exercise training has the potential to protect pancreatic β cells against an immune response in vivo. However, curcumin supplementation failed to attenuate insulitis in NOD mice. ConclusionsThese data provide evidence that exercise training can mitigate T1D development in genetically susceptible mice.
机译:背景自身免疫性发病机制的主要机制是针对自身抗原的不受控制的炎症反应。因此,抗炎因子,例如生物活性化合物的摄入和体育锻炼的生活方式,可能会减少或停止自身免疫性疾病的发展。 1型糖尿病(T1D)是一种以胰腺β细胞破坏为特征的自身免疫性疾病。非肥胖糖尿病(NOD)小鼠是自发性T1D的模型,并且是与人类疾病最相似的模型。方法为了确定运动训练和姜黄素补充对T1D进展的影响,将48只5周大的NOD小鼠随机分为四组:对照组,补充姜黄素,训练后和训练加姜黄素。每2周使用血糖仪测量一次血糖。在20周后,采用组织病理学方法评估免疫细胞是否浸入胰腺β细胞(胰岛炎)。结果中等强度的运动训练有可能保护胰腺β细胞免受体内的免疫反应。但是,补充姜黄素不能减轻NOD小鼠的胰岛炎。结论这些数据提供了运动训练可以减轻遗传易感小鼠T1D发育的证据。

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