卢佩通过NRF2-介导的抗氧化和抗炎作用减弱了氧化醇诱导的树突细胞激活
Sarmistha Saha1,2, Antonella Capozzi3, Elisabetta Profumo1
1Department of Cardiovascular, Endocrine-Metabolic Diseases and Aging, Italian National Institute of Health, 00161 Rome, Italy.
International journal of molecular sciences
|August 14, 2025
概括
卢皮醇是一种天然化合物,促进了宽容性树突细胞 (DCs),并通过激活NRF2通路来减少炎症. 这表明Lupeol是Lupeol.
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.
- 氧化压力研究研究 氧化压力研究
背景情况:
- 像7-基托胆固醇 (7KCh) 这样的氧化醇通过氧化应激和免疫细胞激活来驱动自身免疫和炎症性疾病.
- 树突细胞 (DCs) 对于免疫耐受性至关重要;它们的功能障碍促进了自身免疫.
- 针对DC的天然化合物提供了一种恢复免疫平衡的策略.
研究的目的:
- 调查卢皮醇对暴露于7KCh的人类单细胞衍生的DCs的免疫调节和抗氧化作用.
- 阐明潜在的分子机制,特别是KEAP1-NRF2通路.
主要方法:
- 流细胞计和细胞因子分析以评估DC表型和细胞因子释放.
- 免疫光和西部斑点用于分析NRF2通路激活 (NRF2,HO-1,NQO1).
- 使用NRF2抑制剂 (ML385) 和分子对接/MM/PBSA分析.
主要成果:
- 卢皮醇保留了耐受性DC表型,增加了IL-10和抑制了成熟标志物 (CD83,CD86).
- 卢佩醇抑制了促炎性细胞因子 (IL-1β,IL-12p70) 并促进了调节性T细胞两极分化.
- 卢皮醇激活了KEAP1-NRF2通路,增加了核NRF2和下游目标;这部分受到7KCh诱导的氧化应激的限制.
结论:
- 卢皮醇在DC中表现出显著的抗氧化和免疫调节特性,由NRF2激活介导.
- 卢佩醇促进了宽容性DCs,减轻了炎症反应,表明了治疗潜力.
- 卢皮醇是治疗自身免疫和慢性炎症疾病的有希望的候选药物.
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