Evidence map›Paper›PMID 33215523›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2021

Resveratrol alleviates alveolar epithelial cell injury induced by hyperoxia by reducing apoptosis and mitochondrial dysfunction.

Xiaodan Zhu, Fan Wang, Xiaoping Lei, Wenbin Dong

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-weighted citation impact, top 6% 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, 37 citations in OpenAlex.

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  6. [Role of reactive oxygen species/silent information regulator 1 in hyperoxia-induced bronchial epithelial cell injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 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

4 authors at 1 institution in 1 country.

Xiaodan ZhuDivision of Neonatology, Department of Pediatrics, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.ORCID 0000-0003-2717-4396
Fan WangDivision of Neonatology, Department of Pediatrics, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Xiaoping LeiDivision of Neonatology, Department of Pediatrics, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Wenbin DongDivision of Neonatology, Department of Pediatrics, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Affiliated Hospital of Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bronchopulmonary dysplasia is a severe and long-term pulmonary disease in premature infants. Hyperoxia-induced acute lung injury plays a critical role in bronchopulmonary dysplasia. Resveratrol is a polyphenolic phytoalexin and a natural agonist of Sirtuin 1. Many studies have shown that resveratrol has a protective effect on hyperoxia-induced lung damage, but its specific protective mechanism is still not clear. Further exploration of the possible protective mechanism of resveratrol was the main goal of this study. In this study, human alveolar epithelial cells were used to establish a hyperoxia-induced acute lung injury cell model, and resveratrol (Res or R), the Sirtuin 1 activator SRT1720 (S) and the Sirtuin 1 inhibitor EX-527 (E) were administered to alveolar epithelial cells, which were then exposed to hyperoxia to investigate the role of Res in mitochondrial function and apoptosis. We divided human alveolar epithelial cells into the following groups: (1) the control group, (2) hyperoxia group, (3) hyperoxia+Res20 group, (4) hyperoxia+Res20+E5 group, (5) hyperoxia+Res20+E10 group, (6) hyperoxia+S2 group, (7) hyperoxia+S2+E5 group, and (8) hyperoxia+S2+E10 group. Hyperoxia-induced cell apoptosis and mitochondrial dysfunction were alleviated by Res and SRT1720. Res and SRT1720 upregulated Sirtuin 1, PGC-1α, NRF1, and TFAM but decreased the expression of acetyl-p53 in human alveolar epithelial cells that were exposed to hyperoxia. These findings revealed that Res may alleviated hyperoxia-induced mitochondrial dysfunction and apoptosis in alveolar epithelial cells through the SIRT1/PGC-1a signaling pathway. Thus, Sirtuin 1 upregulation plays an important role in lung protection.

Indexed as

ApoptosisAcetylationAlveolar Epithelial CellsCarbazolesCell DeathCell LineCell SurvivalDNA-Binding ProteinsDown-RegulationHeterocyclic Compounds, 4 or More RingsHumansHyperoxiaMembrane Potential, MitochondrialMitochondriaMitochondrial ProteinsModels, Biological6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamideCarbazolesDNA-Binding ProteinsHeterocyclic Compounds, 4 or More RingsMitochondrial ProteinsNRF1 protein, humanNuclear Respiratory Factor 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReactive Oxygen SpeciesResveratrolSirtuin 1SRT1720TFAM protein, humanTranscription FactorsTumor Suppressor Protein p53apoptosisBronchopulmonary dysplasiaEX-527mitochondrial dysfunctionresveratrolSRT1720

Identifiers

PMID33215523
PMCPMC7934147
OpenAlexW3100239803

What OpenQuestion holds

Textmetadata
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.