林介导的ATPIF1-mTOR信号抑制减轻了辐射诱导的巨细胞极化和结肠炎症
Lei Chang1, Le Zhou2, Shan Jiang2
1Department of Urology, Tongji Medical College, Central Hospital of Wuhan, Huazhong University of Science and Technology, Wuhan, 430014, China.
Inflammation
|February 25, 2026
概括
林补充剂通过ATPIF1-mTOR通路抑制M1巨细胞极化来抵消辐射诱导的炎症. 这一发现为放射性结肠炎提供了潜在的治疗策略.
科学领域:
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
- 代谢过程中的代谢.
背景情况:
- 放射治疗可能会导致炎症并发症,如辐射性结肠炎.
- M1巨细胞极化驱动辐射诱导的炎症.
- 林代谢在这个过程中的作用是未知的.
研究的目的:
- 为了研究素代谢在辐射诱导的M1巨细胞极化和炎症中的作用.
- 探索涉及ATPIF1-mTOR轴的潜在分子机制.
- 在辐射性大肠炎的老鼠模型中评估proline的治疗潜力.
主要方法:
- 暴露在骨髓衍生巨细胞 (BMDMs) 和RAW264.7细胞中的4Gy辐射.
- 补充了细胞和老鼠与proline.
- 分析了巨分化,细胞因子水平,线粒体功能和基因/代谢物表达 (RNA-seq,代谢学).
- 使用了ATPIF1敲击和老鼠辐射结肠炎模型.
主要成果:
- 辐射增加了M1极化,促炎性细胞因子和线粒体功能障碍.
- 林补充剂逆转了这些效应,抑制了M1极化,并恢复了线粒体功能.
- 辐射上调了ATPIF1和p-mTOR; 林使这些正常化.
- 降低ATPIF1模仿了辐射效应,并取消了proline的保护.
- 在老鼠中,proline减轻了结肠损伤和M1透.
结论:
- ATPIF1-mTOR轴是辐射诱导的M1巨细胞极化的一个关键调解器.
- 林补充剂有效地通过这个轴对抗辐射诱导的炎症.
- 林对辐射性大肠炎的治疗有前途.
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