Evidence map›Paper›PMID 39051083›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2024

[Urolithin A alleviates respiratory syncytial virus-induced lung infection in neonatal mice by activating miR-136-mediated Sirt1 signaling].

H Wang, H Xie, W Xu, M Li

Abstract readEnglish Abstract
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

4 authors.

H WangDepartment of Pediatrics, Affiliated Hospital of Inner Mongolia University for Nationalities, Tongliao 028000, China.
H XieDepartment of Pediatrics, Affiliated Hospital of Inner Mongolia University for Nationalities, Tongliao 028000, China.
W XuDepartment of Pediatrics, Affiliated Hospital of Inner Mongolia University for Nationalities, Tongliao 028000, China.
M LiDepartment of Pediatrics, Fourth People's Hospital of Horqin District, Tongliao 028000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo observe the therapeutic effects of urolithin A (UA) on respiratory syncytial virus (RSV)-induced lung infection in neonatal mice and explore the underlying mechanisms.

methodsBabl/c mice (5-7 days old) were subjected to nasal instillation of RSV and received intraperitoneal injection of saline or 2.5, 5 and 10 mg/kg UA 2 h after the infection and then once daily for 2 weeks. Bronchoalveolar lavage fluid (BALF) was then collected for detection of inflammatory cells and mediators, and lung pathology was evaluated with HE staining. RSV-infected BEAS-2B cells were treated with 2.5, 5 or 10 µmol/ L UA. Inflammatory factors, cell viability, apoptosis and autophagy were analyzed using ELISA, CCK-8 assay, TUNEL staining, flow cytometry, Western blotting and immunofluorescence staining. The cellular expressions of miR-136 and Sirt1 mRNAs were detected using qRT-PCR. A dual-luciferase reporter system was used to verify the binding between miR-136 and Sirt1.

resultsIn neonatal Babl/c mice, RSV infection caused obvious lung pathologies, promoted pulmonary cell apoptosis and LC3-Ⅱ/Ⅰ, Beclin-1 and miR-136 expressions, and increased the total cell number, inflammatory cells and factors in the BALF and decreased p62 and Sirt1 expressions. All these changes were alleviated dose-dependently by UA. In BEAS-2B cells, RSV infection significantly increased cell apoptosis, LC3B-positive cells and miR-136 expression and reduced Sirt1 expression (

conclusionUA ameliorates RSV-induced lung infection in neonatal mice by activating miR-136-mediated Sirt1 signaling pathway.

Indexed as

Animals, NewbornApoptosisMice, Inbred BALB CMicroRNAsRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsSignal TransductionSirtuin 1AnimalsAutophagyBronchoalveolar Lavage FluidCoumarinsHumansLungMiceCoumarinsMicroRNAsSirt1 protein, mouseSirtuin 1miR-136respiratory syncytial virusSirt1urolithin A

Identifiers

PMID39051083
PMCPMC11270657

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.