About: Sinensetin suppresses influenza a virus-triggered inflammation through inhibition of NF-κB and MAPKs signalings

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: Sinensetin suppresses influenza a virus-triggered inflammation through inhibition of NF-κB and MAPKs signalings Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Sinensetin suppresses influenza a virus-triggered inflammation through inhibition of NF-κB and MAPKs signalings
Creator	Li, Jing Chen, Ziyu Jie, Xiang Li, Jiashun Liang, Xiaoli Pan, Xiping Xie, Peifang Zhou, Beixian
Source	PMC
abstract	BACKGROUND: Human respiratory system infected with influenza A virus (IAV) elicited a robust pro-inflammatory response that resulted in severe illness and even death. Currently, limited immunomodulator is available to counteract IAV-associated pneumonia in the clinic. Sinensetin, a polymethoxylated flavone with five methoxy groups, has been found to possess anti-agiogenesis, anti-inflammatory and anti-diabetic activities. However, the effects of sinensetin on IAV-triggered pro-inflammatory response remain unclear. In the present study, the anti-inflammatory effects and corresponding possible mechanism of sinensetin in IAV-infected A549 cells were subjected to investigations. METHODS: The cytotoxic effects of sinensetin towards A549 cells was detected by MTT and LDH assays. The antiviral activity of sinensetin against influenza A virus was assayed in A549 cells with an engineered replication-competent influenza A virus carrying Gaussia luciferase reporter gene infection. The effect of sinensetin on influenza A virus-triggered inflammatory reaction was determined by qRT-PCR, Luminex assays, ELISA and Western blot. RESULTS: Our results showed that sinensetin did not exhibit antiviral activity against A/PR/8/34 (H1N1). Meanwhile, sinensetin treatment significantly decreased IAV-induced expression of pro-inflammatory mediators at mRNA and protein levels, including IL-6, TNF-α, IP-10, IL-8 and MCP-1. Additionally, levels of cyclooxygenase (COX)-2 and the downstream product prostaglandin E(2) (PGE(2)) up-regulated by IAV infection were dramatically suppressed by sinensetin. The mechanistic investigation revealed that sinensetin treatment suppressed the NF-κB transcriptional activity using the NF-κB reporter stable HEK293 cell line stimulated with TNF-α (20 ng/mL) or influenza H1N1 virus. Furthermore, sinensetin abrogated influenza H1N1 virus-induced activation of NF-κB, ERK1/2 MAPK and p38 MAPK signalings. CONCLUSION: Collectively, our results indicated that sinensetin has potential capacity to attenuate IAV-triggered pro-inflammatory response via inactivation of NF-κB, ERK1/2 MAPK and p38 MAPK signalings, which implied that sinensetin may be a promising candidate drug for influenza H1N1 virus infection therapeutics.
has issue date	2020-05-05(xsd:dateTime)
bibo:doi	10.1186/s12906-020-02918-3
bibo:pmid	32370749
has license	cc-by
sha1sum (hex)	a44c40cd6e5f432c3cefa74811dfc3ce27a77f29
schema:url	https://doi.org/10.1186/s12906-020-02918-3
resource representing a document's title	Sinensetin suppresses influenza a virus-triggered inflammation through inhibition of NF-κB and MAPKs signalings
has PubMed Central identifier	PMC7200050
has PubMed identifier	32370749
schema:publication	BMC Complement Med Ther
resource representing a document's body	covid:a44c40cd6e5f432c3cefa74811dfc3ce27a77f29#body_text
is schema:about of	named entity 'response' named entity 'influenza A virus' named entity 'PRESENT' named entity 'DIABETIC' named entity 'PNEUMONIA' named entity 'HUMAN' named entity 'A549 CELLS' named entity 'BAB' named entity 'INFLAMMATION' named entity 'mechanism' named entity 'robust' named entity 'effects' named entity 'sinensetin' named entity 'sinensetin' named entity 'polymethoxylated flavone' named entity 'IAV' named entity 'influenza a virus' named entity 'TNF-α' named entity 'one-way ANOVA' named entity 'p38' named entity 'infectious diseases' named entity 'ARDS' named entity 'sinensetin' named entity 'inoculated' named entity 'microplate Reader' named entity 'plasma membrane' named entity 'dimethyl sulfoxide' named entity 'lipid' named entity 'HEK293' named entity 'NF-κB' named entity 'chemokines' named entity 'MAPK' named entity 'Sigma-Aldrich' named entity 'ERK1/2' named entity 'electrophoresed' named entity 'inflammatory response' named entity 'lipid' named entity 'inflammation' named entity 'IAV' named entity 'cDNA' named entity 'TNF-α' named entity 'IAV' named entity 'signaling cascades' named entity 'MAPK' named entity 'influenza' named entity 'sinensetin' named entity 'clinical outcome' named entity 'sinensetin' named entity 'corticosteroids' named entity 'IAV' named entity 'centrifuged' named entity 'TCP' named entity 'P38' named entity 'pharmacological' named entity 'protein' named entity 'RPMI' named entity 'oseltamivir' named entity 'NF-κB' named entity 'IL-6' named entity 'oseltamivir' named entity 'cytotoxic' named entity 'supernatants' named entity 'DMEM' named entity 'ERK1/2' named entity 'retrospective studies' named entity 'antiinflammatory' named entity 'corticosteroids' named entity 'sinensetin' named entity 'Sinensetin' named entity 'infection' named entity 'A549' named entity 'sinensetin' named entity 'immune responses' named entity 'BCA protein assay'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2025 OpenLink Software