Evidence map›Paper›PMID 31077204›Full record

ArticleRespiratory research2019

Antioxidative effects of caffeine in a hyperoxia-based rat model of bronchopulmonary dysplasia.

Stefanie Endesfelder, Evelyn Strauß, Till Scheuer, Thomas Schmitz, Christoph Bührer

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. 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
6.3field-weighted citation impact, top 3% 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, 58 citations in OpenAlex.

  1. Cannabidiol Protects the Neonatal Mouse Heart from Hyperoxia-Induced Injury.International journal of molecular sciences · 2025
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  15. 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 1 institution in 1 country.

Stefanie EndesfelderDepartment of Neonatology, Charité Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany. stefanie.endesfelder@charite.de.ORCID http://orcid.org/0000-0002-4030-7969
Evelyn StraußDepartment of Neonatology, Charité Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Till ScheuerDepartment of Neonatology, Charité Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Thomas SchmitzDepartment of Neonatology, Charité Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Christoph BührerDepartment of Neonatology, Charité Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhile additional oxygen supply is often required for the survival of very premature infants in intensive care, this also brings an increasing risk of progressive lung diseases and poor long-term lung outcomes. Caffeine is administered to neonates in neonatal intensive care for the prevention and treatment of apneas and has been shown to reduce BPD incidence and the need for mechanical ventilation, although it is still unclear whether this is due to a direct pulmonary action via antagonism of adenosine receptors and/or an indirect action. This experimental study aims to investigate the action of caffeine on the oxidative stress response in pulmonary tissue in a hyperoxia-based model of bronchopulmonary dysplasia in newborn rats.

methodsNewborn Wistar rats were exposed to 21% or 80% oxygen for 3 (P3) or 5 (P5) postnatal days with or without recovery on room air until postnatal day 15 (P15) and treated with vehicle or caffeine (10 mg/kg) every 48 h beginning on the day of birth. The lung tissue of the rat pups was examined for oxidative stress response at P3 and P5 immediately after oxygen exposure or after recovery in ambient air (P15) by immunohistological staining and analysis of lung homogenates by ELISA and qPCR.

resultsLungs of newborn rats, corresponding to the saccular stage of lung development and to the human lung developmental stage of preterms, showed increased rates of total glutathione and hydrogen peroxide, oxidative damage to DNA and lipids, and induction of second-phase mediators of antioxidative stress response (superoxide dismutase, heme oxygenase-1, and the Nrf2/Keap1 system) in response to hyperoxia. Caffeine reduced oxidative DNA damage and had a protective interference with the oxidative stress response.

conclusionIn addition to the pharmacological antagonism of adenosine receptors, caffeine appears to be a potent antioxidant and modulates the hyperoxia-induced pulmonary oxidative stress response and thus protective properties in the BPD-associated animal model. Free-radical-induced damage caused by oxidative stress seems to be a biological mechanism progress of newborn diseases. New aspects of antioxidative therapeutic strategies to passivate oxidative stress-related injury should be in focus of further investigations.

Indexed as

Disease Models, AnimalAnimalsAnimals, NewbornAntioxidantsBronchopulmonary DysplasiaCaffeineFemaleHyperoxiaOxidative StressPregnancyRandom AllocationRatsRats, WistarTreatment OutcomeAntioxidantsCaffeineAnimal modelAntioxidantCaffeineHyperoxia (oxygen)Oxidative stressPreterm

Identifiers

PMID31077204
PMCPMC6511176
OpenAlexW2947463202

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LicenceCC BY
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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.