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About:
Anemoside B4 protects against Klebsiella pneumoniae- and influenza virus FM1-induced pneumonia via the TLR4/Myd88 signaling pathway in mice
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covidontheweb.inria.fr
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Academic Article
research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
Anemoside B4 protects against Klebsiella pneumoniae- and influenza virus FM1-induced pneumonia via the TLR4/Myd88 signaling pathway in mice
Creator
He, Jia
Zhao, Yonghui
Cui, Xiaolan
Gao, Hongwei
Chen, Yangling
Cui, Yushun
Han, Shan
Huang, Liting
Wang, Qin-Qin
Xu, Qiongming
Yang, Shilin
Yuan, Renyikun
Source
Medline; PMC
abstract
BACKGROUND: Pneumonia refers to the inflammation of the terminal airway, alveoli and pulmonary interstitium, which can be caused by pathogenic microorganisms, physical and chemical factors, immune damage, and drugs. Anemoside B4, the major ingredient of Pulsatilla chinensis (Bunge) Regel, exhibited anti-inflammatory activity. However, the therapeutic effect of anemoside B4 on pneumonia has not been unraveled. This study aims to investigate that anemoside B4 attenuates the inflammatory responses in Klebsiella pneumonia (KP)- and influenza virus FM1 (FM1)-induced pneumonia mice model. METHODS: The network pharmacology and molecular docking assays were employed to predict the targets of anemoside B4’s treatment of pneumonia. Two models (bacterial KP-infected mice and virus FM1-infected mice) were employed in our study. BALB/c mice were divided into six groups: control, model group (KP-induced pneumonia or FM1-induced pneumonia), anemoside B4 (B4)-treated group (2.5, 5, 10 mg/kg), and positive drug group (ribavirin or ceftriaxone sodium injection). Blood samples were collected for hematology analysis. The effects of B4 on inflammation-associated mediators were investigated by Enzyme-linked immunosorbent assay (ELISA) and hematoxylin and eosin staining (HE) staining. Proteins expression was quantified by western blotting. RESULTS: The network results indicated that many pro-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) participated in anemoside B4’s anti-inflammatory activity. The counts of neutrophil (NEU) and white blood cell (WBC), the level of myeloperoxidase (MPO), and the release of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 increased by KP or FM1 infection, which were reversed by anemoside B4. In addition, anemoside B4 significantly suppressed the FM1-induced expression of toll-like receptor 4 (TLR4), myeloid differential protein-88 (MyD88), and myeloid differentiation protein-2 (MD-2), which were further validated by molecular docking data that anemoside B4 bound to bioactive sites of TLR4. Therefore, anemoside B4 exhibited a significant therapeutic effect on pneumonia via the TLR4/MyD88 pathway. CONCLUSION: Our findings demonstrated that anemoside B4 attenuates pneumonia via the TLR4/Myd88 signaling pathway, suggesting that anemoside B4 is a promising therapeutic candidate for bacterial-infected or viral-infected pneumonia.
has issue date
2020-07-02
(
xsd:dateTime
)
bibo:doi
10.1186/s13020-020-00350-w
bibo:pmid
32625244
has license
cc-by
sha1sum (hex)
96bb88d72ca53c3a41543aaa61d714207765f363
schema:url
https://doi.org/10.1186/s13020-020-00350-w
resource representing a document's title
Anemoside B4 protects against Klebsiella pneumoniae- and influenza virus FM1-induced pneumonia via the TLR4/Myd88 signaling pathway in mice
has PubMed Central identifier
PMC7330533
has PubMed identifier
32625244
schema:publication
Chin Med
resource representing a document's body
covid:96bb88d72ca53c3a41543aaa61d714207765f363#body_text
is
schema:about
of
named entity 'terminal'
named entity 'Pneumonia'
named entity 'This'
named entity 'drugs'
named entity 'model'
named entity 'alveoli'
named entity 'Pulsatilla chinensis'
named entity 'Klebsiella pneumonia'
named entity 'alveoli'
named entity 'TLR4'
named entity 'Klebsiella pneumoniae'
named entity 'pneumonia'
named entity 'antibiotics'
named entity 'Myeloperoxidase'
named entity 'homogenized'
named entity 'control group'
named entity 'TLR4'
named entity 'Beijing'
named entity 'pneumonia'
named entity 'Pneumonia'
named entity 'blood counts'
named entity 'TNF-α'
named entity 'pathogen'
named entity 'pharmacology'
named entity 'pneumonia'
named entity 'cytokine'
named entity 'oxidation'
named entity 'non-invasive'
named entity 'TLR4'
named entity 'pharmacology'
named entity 'antitumor'
named entity 'TLR4'
named entity 'alveolar septum'
named entity 'TLR4'
named entity 'TNF-α'
named entity 'IL-1β'
named entity 'TLR4'
named entity 'Klebsiella pneumoniae'
named entity 'primary antibodies'
named entity 'Chinese Academy of Sciences'
named entity 'TIR'
named entity 'amino acid'
named entity 'pneumonia'
named entity 'optical microscope'
named entity 'pneumonia'
named entity 'IL-1β'
named entity 'TIR'
named entity 'supernatant'
named entity 'Beverly, MA'
named entity 'ethanol'
named entity 'staining'
named entity 'ribavirin'
named entity 'antibody'
named entity 'downstream pathways'
named entity 'pathogens'
named entity 'pneumonia'
named entity 'lung tissue'
named entity 'TLR4'
named entity 'Pulsatilla chinensis'
named entity 'pro-inflammatory cytokines'
named entity 'non-invasive'
named entity 'TLR4'
named entity 'anti-inflammatory'
named entity 'TNF-α'
named entity 'neuraminidase inhibitors'
named entity 'China'
named entity 'hemoglobin'
named entity 'PVDF'
named entity 'cytokines'
named entity 'WBC'
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