Evidence map›Paper›PMID 30862773›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

Effect of Montelukast on Bronchopulmonary Dysplasia (BPD) and Related Mechanisms.

Xin Chen, Xiaoqian Zhang, Jiahua Pan

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Evaluating the role of montelukast on doxorubicin-induced cardiotoxicity in breast cancer patients.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025
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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

3 authors at 3 institutions in 1 country.

Xin ChenDepartment of Pediatrics, The First Hospital Affiliated to Bengbu Medical College, Bengbu, Anhui, China (mainland).
Xiaoqian ZhangDepartment of Children's Health Care, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Maternity and Child Care Hospital, Nanjing, Jiangsu, China (mainland).
Jiahua PanDepartment of Pediatrics, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui, China (mainland).
First Affiliated Hospital of Bengbu Medical College · CNJiangsu Province Hospital · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Bronchopulmonary dysplasia (BPD) is a chronic lung disease common in preterm infants. Montelukast, an effective cysteinyl leukotriene (cysLT) receptor antagonist, has a variety of pharmacological effects and has protective effects against a variety of diseases. Currently, the efficacy and safety of montelukast sodium in treating BPD has been revealed, however, the precise molecular mechanism of the effect of montelukast on BPD development remain largely unclear. Therefore, this study aimed to investigate the effect and mechanism of montelukast on BPD in vivo and in vitro. MATERIAL AND METHODS A mouse BPD model and hyperoxia-induced lung cell injury model were established and treated with montelukast. Then mean linear intercept (MLI), radial alveolar count (RAC), lung weight/body weight (LW/BW) ratio, pro-inflammatory factors, and oxidative stress-related factors in lung tissues were determined. Cell viability and apoptosis were detected using MTT assay and flow cytometer respectively. RESULTS The results showed that montelukast treatment relieved mouse BPD, evidenced by increased RAC and decreased MLI and LW/BW ratios. We also found that montelukast treatment reduced pro-inflammatory factors (TNF-alpha, IL-6, and IL-1ß) production, enhanced superoxide dismutase (SOD) activity, and reduced malondialdehyde (MDA) content in the lung tissues of BPD mice. Besides, montelukast eliminated the reduced cell viability and enhanced cell apoptosis induced by hyperoxia exposure in vitro. Moreover, the upregulated pro-inflammatory factors production and p-p65 protein level in lung cells caused by hyperoxia were decreased by montelukast treatment. CONCLUSIONS Montelukast protected against mouse BPD induced by hyperoxia through inhibiting inflammation, oxidative stress, and lung cell apoptosis.

Indexed as

AcetatesAnimalsAnimals, NewbornApoptosisBronchopulmonary DysplasiaCyclopropanesDisease Models, AnimalHyperoxiaInterleukin-1betaInterleukin-6LungLung InjuryMiceMice, Inbred C57BLOxidative StressQuinolinesAcetatesCyclopropanesInterleukin-1betaInterleukin-6leukotriene D4 receptormontelukastQuinolinesReceptors, LeukotrieneSulfidesTumor Necrosis Factor-alpha

Identifiers

PMID30862773
PMCPMC6427930
OpenAlexW2922290085

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.