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IL-37通过减轻上皮层-介质细胞过渡和促进M2巨细胞极化来改善慢性子宫内膜炎

Zihan Wang¹, Jiaxi Tan¹, Rui Zhang¹

¹School of Medical Technology and Translational Medicine, Hunan Normal University, Tongzipo Road, Changsha 410013, China.

Current issues in molecular biology

|February 27, 2026

概括

干白素-37 (IL-37) 通过减少炎症和组织损伤来缓解慢性子宫内膜炎 (CE). 它抑制了表皮-介质细胞过渡 (EMT) 并促进M2巨细胞两极分化,为CE提供了潜在的治疗益处.

科学领域:

生殖免疫学生殖免疫学
细胞和分子生物学是细胞和分子生物学.

背景情况:

慢性子宫内膜炎 (CE) 是一种炎症性子宫疾病,治疗目标不明.
介素-37 (IL-37) 是一种抗炎性细胞因子,在CE病变发生过程中具有未明确的作用.
表皮-介质细胞过渡 (EMT) 和巨细胞两极分化都与CE有关.

研究的目的:

在CE的老鼠模型中研究IL-37的治疗机制.
为了探索IL-37对EMT和CE的巨细胞极化的影响.
为了阐明参与IL-37的作用的分子途径.

主要方法:

通过使用脂聚糖 (LPS) 诱导CE的老鼠模型,并用IL-37.7治疗.
采用了组织学,免疫光,透孔,qPCR,西部斑块和流动细胞计分析.
评估了STAT6和Smad3通路的激活.

主要成果:

治疗IL-37可以减少子宫炎症,组织损伤和纤维化.
通过对E-cadherin进行上调和对维门丁进行下调,IL-37抑制了EMT.
IL-37抑制了M1巨细胞的两极分化,并促进了M2两极分化.
IL-37协同激活了STAT6和Smad3通路,增加了ARG1的表达.

结论:

通过减轻炎症和组织损伤,IL-37证明了CE的治疗潜力.
通过抑制EMT和促进M2巨细胞极化,IL-37可以改善CE.
STAT6和Smad3通路的协调激活介导了IL-37在CE中的保护作用.

关键词:

介质蛋白-37-37 介质蛋白-37 介质蛋白-37 慢性子宫内膜炎慢性子宫内膜炎表皮介质介质的过渡.巨细胞的两极分化

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