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An active component containing pterodontic acid and pterodondiol isolated from Laggera pterodonta inhibits influenza A virus infection through the TLR7/MyD88/TRAF6/NF‑κB signaling pathway.

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机构: [1]State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease,First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510120 [2]Institute of Tropical Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405 [3]State Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Taipa, Macau SAR 999078 [4]School of Pharmaceutical Science and Biomedical Engineering Research Center, Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, Yunnan 650500 [5]Institute of Chinese Integrative Medicine, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China
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关键词: Laggera pterodonta influenza virus nuclear factor‑κB signaling pathway anti‑inflammatory

摘要:
The influenza virus is a pathogen that can cause pandemic and epidemic outbreaks, and therefore represents a severe threat to human health. Antiviral drugs have an important role in the prevention and treatment of influenza, although the increasing emergence of drug resistance has given rise to a requirement for the development of novel antiviral drugs. In the present study, an active component (C8) isolated from Laggera pterodonta was evaluated. The nuclear magnetic resonance spectroscopy and mass spectrometry analysis results revealed that two eudesmane‑type sesquiterpene compounds were identified in C8; pterodontic acid and pterodondiol. C8 was demonstrated to have a broad‑spectrum effect against different influenza viruses, including human and avian influenza viruses, with a half maximal inhibitory concentration value of 19.9‑91.4 µg/ml. The antiviral mechanisms of C8 were further clarified. Western blot analysis verified that C8 inhibited Toll‑like receptor 7, myeloid differentiation primary response protein 88 and tumor necrosis factor (TNF) receptor associated factor 6 expression, in addition to p65 phosphorylation, at a concentration of 100 or 150 µg/ml. An indirect immunofluorescence assay demonstrated that C8 may inhibit p65/NF‑κB nuclear translocation. Additionally, C8 prevented an increase in cytokine mRNA expression, including interleukin (IL)‑1β, IL‑6, IL‑8 and C‑C motif chemokine 2 (MCP‑1). Furthermore, the Bio‑Plex assay results indicated that the protein expression of IL‑6, IL‑8, TNF‑α, C‑X‑C motif chemokine 10, MCP‑1 and C‑C motif chemokine 5 was inhibited. These findings suggest that C8 has the potential to be developed into an anti‑inflammatory drug for the prevention and treatment of influenza A virus infection.

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出版当年[2018]版:
大类 | 4 区 医学
小类 | 4 区 医学:研究与实验 4 区 肿瘤学
最新[2023]版:
大类 | 3 区 医学
小类 | 4 区 医学:研究与实验 4 区 肿瘤学
第一作者:
第一作者机构: [1]State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease,First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510120
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通讯作者:
通讯机构: [1]State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease,First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510120 [*1]State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang Road, Guangzhou, Guangdong 510120, P.R. China
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