奎瑞通过TLR4/IRAK4/NF-κB信号通路抑制树突细胞的活性和功能
Chenglin Kang1,2,3, Xiaomei Li3, Peng Liu1,2
1Department of Graduate and Scientific Research, Zunyi Medical University Zhuhai Campus, Zhuhai, People's Republic of China.
概括
奎尔赛丁 (QUE) 通过向类似收费受体4/互乐金-1受体关联激酶4/核因子kappa-B (TLR4/IRAK4/NF-κB) 途径来抑制树突细胞 (DC) 的活性. 这表明IRAK4是调节DC功能的潜在治疗标.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 树突细胞 (DCs) 在免疫反应中起着至关重要的作用.
- 电流活动的失调与各种炎症状况有关.
- 鉴定DC激活的新型抑制剂对于治疗开发至关重要.
研究的目的:
- 研究奎尔素 (QUE) 对树突细胞 (DC) 的抑制作用.
- 阐明涉及收费类受体4/介质素-1受体关联激酶4/核因子kappa-B (TLR4/IRAK4/NF-κB) 信号通路的潜在分子机制.
- 在DC中识别Quercetin的潜在分子标.
主要方法:
- 细胞活力和细胞亡测定 (CCK-8) 以确定最佳的QUE度和时间.
- 西部涂抹测试用于评估TLR4,IRAK4和NF-κB p65.5的蛋白质表达水平.
- 流细胞计分析DC上的表面标记物表达 (CD86,CD11c).
- 分子对接以预测QUE和IRAK之间的结合相互作用4.
主要成果:
- 奎尔素以时间和剂量依赖的方式抑制了DC活性和功能.
- Quercetin 治疗降低了 TLR4,IRAK4 和 NF-κB p65 蛋白质的表达.
- 奎瑞降低了DC表面标记物CD86和CD11c的脂聚糖 (LPS) 诱导的表达.
- 分子对接表明QUE与IRAK4的稳定结合,这表明IRAK4是潜在的目标.
结论:
- 奎尔对树突细胞活动和功能表现出抑制作用.
- 该机制涉及TLR4/IRAK4/NF-κB信号通路的调制.
- 鉴定出IRAK4 (互乐金-1受体关联激酶4) 是奎尔塞丁对DCs作用的潜在分子标.
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