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从烈香杜鹃中分离得到的五种新杂萜及其抗炎活性。

Five new meroterpenoids from Rhododendron anthopogonoides and their anti-inflammatory activity.

作者信息

Li Mengtian, Kelsang Norbu, Zhao Yongqin, Li Wensen, Zhou Feng, Cui Lu, Bao Xianjie, Wang Qian, Feng Xin, Yang Minghua

机构信息

State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China.

Tibet Ganlu Pharmaceutical Technology Company, Lhasa 850032, China; Technological Innovation Center of Traditional Tibetan Medicine Modernization of Tibet Autonomous Region, Lhasa 850032, China.

出版信息

Chin J Nat Med. 2025 Jul;23(7):881-887. doi: 10.1016/S1875-5364(25)60850-8.

DOI:10.1016/S1875-5364(25)60850-8
PMID:40653328
Abstract

Five meroterpenoids, rhodonoids K-M (1-2), daurichromene E (3), and grifolins A-B (4-5), together with seven known compounds (6-12), were isolated from Rhododendron anthopogonoides. The chemical structures of these compounds were elucidated through comprehensive analysis of high-resolution electrospray ionization mass spectrometry (HR-ESI-MS), ultraviolet (UV), infrared spectroscopy (IR), and nuclear magnetic resonance (NMR) data. Their absolute configurations were determined by comparing experimental electronic circular dichroism (ECD) spectra with computed values. Notably, compounds 1 and 3 demonstrated significant inhibitory effects on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 cells. These compounds markedly suppressed the mRNA expressions of inflammatory factors, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) while also down-regulating the protein expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2).

摘要

从烈香杜鹃中分离得到了5个半萜类化合物,即杜鹃素K-M(1-2)、牛儿基香豆素E(3)和松萝酸A-B(4-5),以及7个已知化合物(6-12)。通过对高分辨电喷雾电离质谱(HR-ESI-MS)、紫外光谱(UV)、红外光谱(IR)和核磁共振(NMR)数据的综合分析,阐明了这些化合物的化学结构。通过将实验性电子圆二色光谱(ECD)与计算值进行比较,确定了它们的绝对构型。值得注意的是,化合物1和3对脂多糖(LPS)诱导的RAW264.7细胞炎症具有显著的抑制作用。这些化合物显著抑制了包括白细胞介素(IL)-1β、IL-6和肿瘤坏死因子-α(TNF-α)在内的炎症因子的mRNA表达,同时还下调了诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的蛋白表达。

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