Evidence map›Paper›PMID 26156213›Full record

ArticleScientific reports2015

Galangin attenuates airway remodelling by inhibiting TGF-β1-mediated ROS generation and MAPK/Akt phosphorylation in asthma.

Ya-Nan Liu, Wang-Jian Zha, Yuan Ma, Fei-Fei Chen, Wen Zhu, Ai Ge, Xiao-Ning Zeng, Mao Huang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
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  19. Effects ofDrug design, development and therapy · 2022
    Article
  20. Ginger-derived compounds exertExperimental and therapeutic medicine · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Ya-Nan LiuDepartment of Respiratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wang-Jian ZhaDepartment of Respiratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yuan MaDepartment of Respiratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Fei-Fei ChenDepartment of Respiratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wen ZhuDepartment of Respiratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ai GeDepartment of Respiratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xiao-Ning ZengDepartment of Respiratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Mao HuangDepartment of Respiratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Galangin, a natural flavonol, has attracted much attention for its potential anti-inflammatory properties. However, its role in the regulation of airway remodelling in asthma has not been explored. The present study aimed to elucidate the effects of galangin on chronic inflammation and airway remodelling and to investigate the underlying mechanisms both in vivo and in vitro. Ovalbumin (OVA)-sensitised mice were administered with galangin 30 min before challenge. Our results showed that severe inflammatory responses and airway remodelling occurred in OVA-induced mice. Treatment with galangin markedly attenuated the leakage of inflammatory cells into bronchoalveolar lavage fluid (BALF) and decreased the level of OVA-specific IgE in serum. Galangin significantly inhibited goblet cell hyperplasia, collagen deposition and α-SMA expression. Lowered level of TGF-β1 and suppressed expression of VEGF and MMP-9 were observed in BALF or lung tissue, implying that galangin has an optimal anti-remodelling effect in vivo. Consistently, the TGF-β1-induced proliferation of airway smooth muscle cells was reduced by galangin in vitro, which might be due to the alleviation of ROS levels and inhibition of MAPK pathway. Taken together, the present findings highlight a novel role for galangin as a promising anti-remodelling agent in asthma, which likely involves the TGF-β1-ROS-MAPK pathway.

Indexed as

ActinsAirway RemodelingAnimalsAsthmaBronchoalveolar Lavage FluidCell ProliferationCollagenDisease Models, AnimalFemaleFibrosisFlavonoidsGoblet CellsHumansHyperplasiaImmunoglobulin EMatrix Metalloproteinase 9Actinsalpha-smooth muscle actin, mouseCollagenFlavonoidsgalanginImmunoglobulin EMatrix Metalloproteinase 9Mitogen-Activated Protein KinasesOvalbuminProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTransforming Growth Factor beta1Vascular Endothelial Growth Factor A

Identifiers

PMID26156213
PMCPMC4496730
OpenAlexW2257472164

What OpenQuestion holds

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Registered trials

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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.