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多免疫代谢矿:NP通过抑制Leucine/PI3K/Akt/mTOR信号通路来预防ALI中的超免疫性

Mantong Zhao¹, Jiazi Lin¹, Xiao Wang¹

¹Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, Department of Biology, Faculty of Arts and Sciences, Beijing Normal University, Zhuhai, 519087, China; School of Chinese Materia Medica, Guangdong Pharmaceutical University, Guangzhou, 510006, China.

Free radical biology & medicine

|October 6, 2024

概括

尼坎德拉植物提取物 (NPE) 通过重塑免疫代谢和抑制炎症,防止急性肺损伤 (ALI). 它调节了Leucine/PI3K/Akt/mTOR通路,抑制了有害的免疫细胞分化.

科学领域:

免疫学免疫学免疫学
药理学药理学是指药理学的学科.
代谢学代谢学代谢学

背景情况:

急性肺损伤 (ALI) 是一个重大的全球健康挑战.
在中国传统医学中使用的Nicandra physalodes (NP) 对ALI具有潜在的治疗特性,但其机制尚不清楚.

研究的目的:

调查尼坎德拉植物提取物 (NPE) 对小鼠的脂多糖 (LPS) 诱导的ALI的保护作用和分子机制.
阐明免疫代谢和特定信号通路在NPE治疗作用中的作用.

主要方法:

网络药理学预测了活性成分和途径.
UPLC-Q-TOF-MS/MS分析了NPE的组成.
(1) H-NMR 免疫代谢剂评估了肺部,血清和便组织的代谢变化.
IHC,IF,RT-qPCR和ELISA验证了关键的蛋白质和基因表达.

主要成果:

NPE含有尼坎德伦,维他诺化物A和贝卡林.
在ALI小鼠中,NPE治疗减少了肺损伤,胀和炎症细胞透.
通过PI3K/Akt/mTOR通路,NPE增强了自和抑制了由Th1/Th17细胞驱动的炎症.
免疫代谢分析显示,NPE通过重塑免疫代谢来逆转ALI诱导的白蛋白抗性.

结论:

通过重塑免疫代谢和调节Leucine/PI3K/Akt/mTOR信号通路,NPE显示出对ALI的保护作用.
NPE 抑制了 Th1/Th17 细胞分化,为其在治疗 ALI 的临床使用提供了科学依据.

关键词:

急性肺损伤是什么?急性肺损伤是什么?自自是一种自的过程.免疫甲基基博洛米克炎症炎症是一种炎症.叶氨酸 (Leucine) 是一种蛋白质.尼坎德拉植物 (Nicandra physalodes) 是一种植物.

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