Evidence map›Paper›PMID 32513156›Full record

ArticleRespiratory research2020

Caffeine prevents hyperoxia-induced lung injury in neonatal mice through NLRP3 inflammasome and NF-κB pathway.

Shangqin Chen, Qiuping Wu, Dingjuan Zhong, Changchong Li, Lizhong Du

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  16. Caffeine and neonatal acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2024
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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

5 authors at 2 institutions in 1 country.

Shangqin ChenDepartment of Pediatrics, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Zhejiang, Hangzhou, China.
Qiuping WuDepartment of Pediatrics, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Zhejiang, Hangzhou, China.
Dingjuan ZhongMolecular Center for Ophthalmic Optics, Hunan Provincial People's Hospital, Changsha, China.
Changchong LiDepartment of Pediatric Pulmonology, The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Lizhong DuDepartment of Pediatrics, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Zhejiang, Hangzhou, China. dulizhong@zju.edu.cn.ORCID http://orcid.org/0000-0002-3181-810X
Wenzhou Medical University · CNChildren's Hospital of Zhejiang University · CN

Funding

National Natural Science Foundation of China 81471480,81630037
6 · The paper itself

Abstract

backgroundBronchopulmonary dysplasia (BPD) is a common chronic lung disease in premature infants and hyperoxia exposure is a major cause. In hyperoxic lung injury animal model, alveolar simplification and pro-inflammatory cells infiltration are the main pathophysiologic changes. Caffeine is a drug used to treat apnea in premature infants. Early use of caffeine can decrease the rate and the severity of BPD while the mechanisms are still unclear. The purpose of this study was to evaluate the effects of caffeine on inflammation and lung development in neonatal mice with hyperoxic lung injury and to explore the possible mechanism.

methodsFollowing 14 d of 75% oxygen exposure in newborn mouse, the BPD model was established. Caffeine at a dose of 1 g/L was added in drinking water to nursing mouse. We measured the concentration of caffeine in serum and oxidative stress in lung by commercially available kits. Adenosine 2A receptor (A

resultsWe found that the caffeine concentration in plasma at present dose significantly decreased the expression of A

conclusionCaffeine treatment can protect hyperoxia-induced mice lung from oxidative injury by inhibiting NLRP3 inflammasome and NF-κB pathway.

Indexed as

AnimalsAnimals, NewbornApoptosisCaffeineDisease Models, AnimalHyperoxiaInflammasomesLung InjuryMiceNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressPhosphodiesterase InhibitorsSignal TransductionCaffeineInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinPhosphodiesterase InhibitorsBronchopulmonary dysplasiaCaffeineInflammasomeNF-κB pathwayOxidative stress

Identifiers

PMID32513156
PMCPMC7278162
OpenAlexW3034034740

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.