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miR-335-3p通过IGF-1调节巨细胞两极分化来改善II型糖尿病

Zhengzheng Ju¹, Fan Cui¹, Zheng Mao¹

¹Department of Clinical Laboratory, Wuhu Hospital Affiliated to Anhui University of Science and Technology (The First People's Hospital of Wuhu), Wuhu, Anhui, China.

Open medicine (Warsaw, Poland)

|March 11, 2024

概括

微RNA-335-3p通过调节胰岛素抵抗和巨细胞两极分化,在第二类糖尿病 (T2DM) 中起着至关重要的作用. 较低的miR-335-3p水平会使T2DM恶化,而增加它们会改善代谢健康.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

微RNA-335 (miR-335) 与II型糖尿病 (T2DM) 模型和胰岛素分泌有关.
关于miR-335-3p在T2DM相关的胰岛素抵抗和巨细胞两极分化中的特定作用的研究有限.

研究的目的:

研究miR-335-3p对T2DM患者胰岛素耐药性和巨细胞两极分化的调节作用.
阐明 miR-335-3p 对 T2DM 病原发生的影响的分子机制.

主要方法:

使用T2DM小鼠模型来评估体重和血糖水平 (葡萄糖耐受性测试,胰岛素耐受性测试).
脂肪组织巨细胞被分离并使用免疫光学,qPCR和西方斑点分析以检测极化标记物 (F4/80,iNOS,TNF-α,IL-10,ARG-1).
生物信息学和双化酶测定证实了miR-335-3p和胰岛素样生长因子1 (IGF-1) 之间的向关系.

主要成果:

在T2DM模型的脂肪组织中,miR-335-3p表达显著下降.
降低miR-335-3p与体重增加和血糖水平相关.
miR-335-3p抑制了巨细胞的增殖和M1极化 (iNOS,TNF-α),同时促进了M2极化 (IL-10,ARG-1).
miR-335-3p直接针对IGF-1,而IGF-1加剧了M1极化和胰岛素抵抗标志物.

结论:

miR-335-3p通过IGF-1通路调节巨细胞极化,作为T2DM中的保护因子.
恢复miR-335-3p水平可能为管理T2DM及其相关并发症提供治疗策略.

关键词:

在IGF-1的基础上,IGF-1 巨细胞的两极分化在 miR-335-3p 中使用.第二种类型的糖尿病.

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