收费样受体 4/变异髓系分化初级反应 88/核因子卡巴-B 介导的炎症在糖尿病伴西北干燥综合征中的作用。

Deng Deqiang, Xiao Yan, M A Dan, Qiu Jinling, Hao Congli, Wang Di, Zhang Miao
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引用次数: 0

摘要

目的研究收费样受体4(TLR4)/突变髓系分化初级反应88(MyD88)/核因子卡巴-B(NF-κB)信号通路介导的炎症在糖尿病合并西北干燥综合征中的作用:将大鼠随机分为正常对照组、2型糖尿病(T2DM)模型组、西北干燥综合征+T2DM(西北干燥)组和单纯内湿+T2DM(内湿)组。采用酶联免疫吸附试验检测生化指标和炎症因子。进行组织病理学观察。采用实时定量聚合酶链反应和 Western 印迹分析分别检测 mRNA 和蛋白质的表达水平:结果:与 T2DM 组相比,内湿组的糖化血红蛋白 A1c、胰岛素、糖耐量、胰岛素抵抗稳态模型评估、肿瘤坏死因子-α、白细胞介素 1β、白细胞介素 16、丙二醛、血脂、丙氨酸氨基转移酶和天冬氨酸氨基转移酶均显著升高,而东北组则显著升高。与 T2DM 组和体内潮湿组相比,西北干燥组的这些指标明显升高。体内潮湿组和西北干燥组的超氧化物歧化酶、谷胱甘肽过氧化物酶、肝糖原和器官重量比明显低于 T2DM 组。但是,西北干燥组的这些水平高于内湿组。此外,干扰素调节因子 5 和 NF-κB p65 的 mRNA 表达水平,以及 TLR4、MyD88 和 NF-κB 的蛋白表达水平在体内潮湿组和西北干燥组均显著高于 T2DM 组。此外,西北干燥组的 mRNA 和蛋白质水平也明显高于内湿组:西北干燥综合征介导的 TLR4/MyD88/NF-κB 通路和慢性炎症可能与 T2DM 的发生和发展有关。
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Role of toll-like receptor 4/mutant myeloid differentiation primary response 88/nuclear factor kappa-B mediated inflammation in diabetes mellitus with Northwest dryness syndrome.

Objective: To investigate the role of toll-like receptor 4 (TLR4)/mutant myeloid differentiation primary response 88 (MyD88)/nuclear factor kappa-B (NF-κB) signaling pathway-mediated inflammation in diabetes mellitus with Northwest dryness syndrome.

Methods: Rats were randomly divided into the normal control, type 2 diabetes (T2DM) model, Northwest dryness syndrome + T2DM (Northwest dryness), and simple internal dampness + T2DM (internal dampness) groups. Enzyme-linked immunosorbent assay was used to detect biochemical indexes and inflammatory factors. The histopathological observation was performed. Quantitative real-time polymerase chain reaction and Western blot analysis were used to detect the mRNA and protein expression levels, respectively.

Results: Compared with the T2DM group, the glycosylated hemoglobin A1c, insulin, glucose tolerance, the homeostasis model assessment of insulin resistance, tumor necrosis factor-α, interleukin 1β, interleukin 16, malondialdehyde, blood lipid, alanine aminotransferase, and aspartate aminotransferase were significantly elevated in the internal dampness group. Their levels were significantly elevated in the Northwest dryness group than in the T2DM and internal dampness groups. The superoxide dismutase, glutathione peroxidase, liver glycogen, and organ-to-weight ratio were significantly declined in the internal dampness group and the Northwest dryness group than in the T2DM group. However, these levels were elevated in the Northwest dryness group than in the internal dampness group. Moreover, the mRNA expression levels of interferon regulatory factor 5 and NF-κB p65, and the protein expression levels of TLR4, MyD88, and NF-κB were significantly higher in the internal dampness and the Northwest dryness groups than the T2DM group. Additionally, the mRNA and protein levels were significantly higher in the Northwest dryness group than in the internal dampness group.

Conclusion: Northwest dryness syndrome-mediated TLR4/MyD88/NF-κB pathway and chronic inflammation might be associated with the occurrence and development of T2DM.

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