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干白素-37通过抑制MAPK/NLRP3通路,促进糖尿病小鼠的伤口愈合

Qiaoli Cui¹, Zhenming Zhang², Lang Qin³

¹Department of Endocrinology, Huashan Hospital, Fudan University, Shanghai, China.

Journal of diabetes investigation

|December 23, 2024

概括

介素-37 (IL-37) 通过抑制炎症,显著加速糖尿病伤口愈合. 这项研究证明了IL-37的存在.

科学领域:

伤口治愈研究研究伤口治愈研究
免疫学免疫学免疫学
糖尿病学糖尿病学

背景情况:

糖尿病足 (DFU) 是一种常见的糖尿病并发症,具有愈合障碍.
介素-37 (IL-37) 是一种已知的先天性炎症抑制剂.

研究的目的:

研究IL-37在增强糖尿病伤口愈合方面的潜力.
探索IL-37在糖尿病伤口中调节炎症通路的机制.

主要方法:

收集了DFU和非糖尿病患者的皮肤样本.
通过使用CRISPR/Cas9.9生成IL-37转基因小鼠 (IL-37Tg).
在小鼠中诱导糖尿病与链毒素 (STZ) 和创建的切割伤口.

主要成果:

在DFU患者中,增强了促炎性细胞因子 (TNF-α,IL-1β) 和MAPK通路激活.
与糖尿病小鼠相比,糖尿病IL-37Tg小鼠表现出加速的伤口愈合.
IL-37抑制了MAPK和NOD类信号通路,减少了TNF-α,IL-1β和NLRP3的表达.

结论:

在糖尿病患者中,IL-37显示出促进皮肤伤口愈合的治疗潜力.
IL-37代表了糖尿病伤口治疗的有前途的新标.

关键词:

在IL-37中,我们可以找到IL-37.炎症炎症是一种炎症.伤口愈合伤口愈合

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