Evidence map›Paper›PMID 29277898›Full record

ArticleClinical and experimental immunology2018

Glucose-6-phosphate dehydrogenase inhibition attenuates acute lung injury through reduction in NADPH oxidase-derived reactive oxygen species.

A Nadeem, N O Al-Harbi, S F Ahmad, K E Ibrahim, N Siddiqui, M M Al-Harbi

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Article in Clinical and experimental immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 59 citations in OpenAlex.

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  9. Glucose-6-Phosphate Dehydrogenase Deficiency and Coronavirus Disease 2019.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023
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  14. Observational
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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

6 authors at 3 institutions in 2 countries.

A NadeemDepartment of Pharmacology and Toxicology, College of Pharmacy, Riyadh, Saudi Arabia.ORCID 0000-0003-2038-8367
N O Al-HarbiDepartment of Pharmacology and Toxicology, College of Pharmacy, Riyadh, Saudi Arabia.
S F AhmadDepartment of Pharmacology and Toxicology, College of Pharmacy, Riyadh, Saudi Arabia.
K E IbrahimDepartment of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
N SiddiquiAmity Institute of Biotechnology, Amity University, Noida, India.
M M Al-HarbiDepartment of Pharmacology and Toxicology, College of Pharmacy, Riyadh, Saudi Arabia.
Riyadh Elm University · SAAmity University · INKing Saud University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI) is a heterogeneous disease with the hallmarks of alveolar capillary membrane injury, increased pulmonary oedema and pulmonary inflammation. The most common direct aetiological factor for ALI is usually parenchymal lung infection or haemorrhage. Reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) are thought to play an important role in the pathophysiology of ALI. Glucose-6-phosphate dehydrogenase (G6PD) plays an important role both in production of ROS as well as their removal through the supply of NADPH. However, how G6PD modulation affects NOX2-mediated ROS in the airway epithelial cells (AECs) during acute lung injury has not been explored previously. Therefore, we investigated the effect of G6PD inhibitor, 6-aminonicotinamide on G6PD activity, NOX2 expression, ROS production and enzymatic anti-oxidants in AECs in a mouse model of ALI induced by lipopolysaccharide (LPS). ALI led to increased G6PD activity in the AECs with concomitant elevation of NOX2, ROS, SOD1 and nitrotyrosine. G6PD inhibitor led to reduction of LPS-induced airway inflammation, bronchoalveolar lavage fluid protein concentration as well as NOX2-derived ROS and subsequent oxidative stress. Conversely, ALI led to decreased glutathione reductase activity in AECs, which was normalized by G6PD inhibitor. These data show that activation of G6PD is associated with enhancement of oxidative inflammation in during ALI. Therefore, inhibition of G6PD might be a beneficial strategy during ALI to limit oxidative damage and ameliorate airway inflammation.

Indexed as

Acute Lung InjuryAnimalsCells, CulturedDisease Models, AnimalFlow CytometryGene Expression RegulationGlucosephosphate DehydrogenaseHumansLipopolysaccharidesMaleMiceMice, Inbred BALB CNADPH OxidasesNiacinamideOxidative StressReactive Oxygen SpeciesGlucosephosphate DehydrogenaseLipopolysaccharidesNADPH OxidasesNiacinamideReactive Oxygen Speciesacute lung injuryairway epithelial cellsG6PD inhibitorNOX2reactive oxygen species

Identifiers

PMID29277898
PMCPMC5801495
OpenAlexW2780415691

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.