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印-3-酸通过巨细胞的糖脂代谢缓解小鼠的DSS诱导的大肠炎

Jiahong Li¹, Peicen Zou², Ruiqi Xiao²

¹Beijing Children Hospital, Capital Medical University, Beijing 100045, China.

International immunopharmacology

|March 14, 2025

概括

印-3-酸 (IPA) 通过重新编程肠道巨细胞,有效治疗性结肠炎 (UC). 这种微生物代谢物将巨细胞从炎症M1转移到抗炎M2,为UC提供了一种新的治疗策略.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
代谢过程中的代谢.

背景情况:

性结肠炎 (UC) 是一种慢性炎症性肠病,治疗选择有限.
巨细胞两极分化和新陈代谢是UC的新兴治疗点.
肠道微生物代谢物英多尔-3-酸 (IPA) 具有抗炎性质.

研究的目的:

研究IPA改善小鼠结肠炎的机制,重点关注巨细胞两极分化和新陈代谢.
在体外和体内探索IPA对M1和M2巨细胞极化的影响.
阐明IPA对巨细胞葡萄糖和脂质代谢途径的影响.

主要方法:

大肠炎的小鼠模型由硫酸德克斯诱导,用口服IPA治疗.
在体外研究使用RAW264.7细胞诱导到带有LPS的M1巨细胞中,并用IPA治疗.
对巨细胞两极分化,JNK/MAPK通路,糖解,脂肪酸氧化以及相关的基因/蛋白质表达 (CPT1A,ACSL1,PPAR-γ) 的分析.

主要成果:

在小鼠中,IPA治疗通过抑制结肠M1巨分化和促进M2分化来改善结肠炎.
在体外,IPA通过JNK/MAPK通路抑制了M1巨细胞的两极分化,抑制了糖分解.
IPA通过上调CPT1A和ACSL1,可能通过PPAR-γ激活来增强M2巨细胞极化和脂肪酸氧化.

结论:

IPA通过调节巨细胞的葡萄糖和脂质代谢来改善结肠炎.
准肠道巨细胞代谢是一种有前途的治疗策略,用于性结肠炎.
IPA调节巨细胞极化和新陈代谢的能力为UC治疗提供了一种新的方法.

关键词:

脂肪酸氧化过程中的脂肪酸氧化.葡萄糖溶解是什么? 葡萄糖溶解印度尔-3-propionic 的使用.巨细胞的新陈代谢性结肠炎是一种

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