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伊卡里西德II通过调节巨细胞极化来减轻白血素诱导的肺纤维化

Lingling Deng¹, Boshu Ouyang¹, Hanlin Shi¹

¹Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, China; Institute of Integrative Medicine, Fudan University, Shanghai, China.

Journal of ethnopharmacology

|June 18, 2023

概括

伊卡里西德II (ISE II) 通过抑制亲纤维M2巨细胞极化,可能通过WNT/β-catenin通路,显示了肺纤维化治疗潜力.

科学领域:

药理学和中国传统医学
细胞生物学和信号传递
肺部医学和纤维化研究

背景情况:

伊卡里因及其代谢物伊卡里西德II (ISE II) 在预防包括纤维化在内的慢性疾病方面表现有前途.
ISE II 具有抗炎和抗氧化特性,可以防止肺部重塑.
目前对ISE II在治疗肺纤维化中的疗效的研究是有限的.

研究的目的:

评估ISE II在肺纤维化模型中的治疗有效性.
研究ISE II在相关细胞信号通路中的作用机制.

主要方法:

在体外 (含TGF-β1的NIH-3T3细胞) 和体内 (白素诱导) 肺纤维化模型中建立.
通过Western blot,RT-qPCR,肺功能测试,微型CT和生物化学测试来评估ISE II的影响.
通过免疫光,流细胞计和转录学来研究机制,重点关注巨细胞极化和WNT/β-catenin信号传递.

主要成果:

ISE II抑制了TGF-β1诱导的α-SMA和纤维细胞中的原蛋白生产.
在小鼠中,ISE II改善了肺功能,减少了原沉积,并降低了促炎细胞因子 (IL-1β,TNF-α,TGF-β1,PDGF).
ISE II减弱了M2巨细胞透和M2标记基因表达,特别是在间歇性巨细胞 (IMs) 中,并抑制了WNT/β-catenin通路激活.

结论:

ISE II通过抑制亲纤维细胞巨分化,在肺纤维化中表现出抗纤维性作用.
治疗机制涉及WNT/β-catenin信号通路的调节,特别是抑制IMs中的M2程序.

关键词:

纤维细胞分化的差异化巨细胞的两极分化肺部纤维化肺部纤维化文字转录学 (Transcriptomics) 是一个学科.通过WNT信号通路传递信号.

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