黄花蒿中二萜内酯二聚体通过激活自噬抑制巨噬细胞中白细胞介素-1β的产生。
Sesquiterpene lactone dimers from Artemisia lavandulifolia inhibit interleukin-1β production in macrophages through activating autophagy.
机构信息
State Key Laboratory of Drug Research, & Natural Products Chemistry Department, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China; School of Life Science and Technology, ShanghaiTech University, Shanghai 201203, China; University of Chinese Academy of Sciences, No. 19A Yuquan Road, Beijing 100049, China.
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Taipa, Macao 999078, China.
出版信息
Bioorg Chem. 2020 Dec;105:104451. doi: 10.1016/j.bioorg.2020.104451. Epub 2020 Nov 4.
Twelve new sesquiterpene lactone dimers, lavandiolides A-L (1-12), were isolated from the whole plants of Artemisia lavandulifolia. Among them, compounds 1-6 are 1,3-linked Diels-Alder adducts between two guaianolide monomers, and 7-12 are 2,4-linked sesquiterpene lactone dimers. Their structures were elucidated by comprehensive analysis of HRESIMS, 1D and 2D NMR spectra. Their absolute configurations were determined by ECD spectra and single-crystal X-ray diffraction analyses with Cu Kα radiation. The nitric oxide (NO) inhibitory effect of all the isolates was assessed on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Compounds 1, 3, 7 and 9 showed potent inhibitory effects on NO production, with IC values of 0.61 ± 0.15, 1.64 ± 0.04, 1.89 ± 0.16, and 1.40 ± 0.23 μM, respectively. Furthermore, compound 1 inhibited NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome-mediated interleukin-1β (IL-1β) production through activating autophagy.
从薰衣草全草中分离得到 12 个新的倍半萜内酯二聚体，命名为 lavandiolides A-L（1-12）。其中，化合物 1-6 是两个愈创木烷内酯单体通过 1,3-二烯加成形成的二聚体，化合物 7-12 是 2,4-连接的倍半萜内酯二聚体。通过高分辨质谱、一维和二维核磁共振谱等综合分析确定了它们的结构。通过圆二色谱和单晶 X 射线衍射分析确定了它们的绝对构型。采用 LPS 刺激 RAW264.7 巨噬细胞法评估了所有分离物对一氧化氮（NO）的抑制作用。化合物 1、3、7 和 9 对 NO 生成表现出很强的抑制作用，IC 值分别为 0.61±0.15、1.64±0.04、1.89±0.16 和 1.40±0.23 μM。此外，化合物 1 通过激活自噬抑制 NLRP3（NOD、LRR 和 pyrin 结构域包含蛋白 3）炎症小体介导致炎因子 1β（IL-1β）的产生。
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