Evidence map›Paper›PMID 35801580›Full record

ArticleRedox report : communications in free radical research2022

Sevoflurane reduces lipopolysaccharide-induced apoptosis and pulmonary fibrosis in the RAW264.7 cells and mice models to ameliorate acute lung injury by eliminating oxidative damages.

Fushuang Zheng, Xiuying Wu, Jin Zhang, Zhiling Fu, Yan Zhang

Open access · goldAbstract read
In one paragraph

Article in Redox report : communications in free radical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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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.

Fushuang ZhengDepartment of Thoracic Surgery, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
Xiuying WuDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
Jin ZhangDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
Zhiling FuDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
Yan ZhangDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.ORCID 0000-0001-8711-4999
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSevoflurane is identified as an effective candidate drug for acute lung injury (ALI) treatment, but its curing effects and detailed mechanisms have not been fully disclosed. The present study was designed to resolve this academic issue.

methodsThe ALI mice models were established, and Hematoxylin-eosin staining assay was performed to examine tissue morphologies. Cell viability was determined by CCK-8 assay, and Annexin V-FITC/PI double staining assay was used to examine cell apoptosis. The expression levels of proteins were determined by performing Western Blot analysis and immunofluorescence staining assay. ROS levels were examined by using DCFH-DA staining assay.

resultsIn this study, we investigated this issue and the ALI models were respectively established by treating the BALB/c mice and the murine macrophage cell line RAW264.7 with different concentrations of lipopolysaccharide (LPS) in vivo and in vitro, which were subsequently subjected to sevoflurane co-treatment. The results showed that sevoflurane reduced LPS-induced ALI in mice and suppressed LPS-triggered oxidative stress and apoptotic cell death in the RAW264.7 cells. Interestingly, we evidenced that the elimination of reactive oxygen species (ROS) by N-acetyl-L-cysteine (NAC) reversed LPS-induced cell apoptosis in RAW264.7 cells. Then, we verified that sevoflurane suppressed oxidative damages to restrain LPS-induced apoptotic cell death in the RAW264.7 cells through activating the anti-oxidant Keap1/Nrf2 pathway. Mechanistically, sevoflurane down-regulated Keap1 and upregulated Nrf2 in nucleus to activate the downstream anti-oxidant signaling cascades, which further ameliorated LPS-induced cell apoptosis and lung injury by eliminating oxidative damages. DISCUSSION: Taken together, our study illustrated that the sevoflurane attenuates LPS-induced ALI by inhibiting oxidative stress-mediated apoptotic cell death and inflammation, and the Keap1/Nrf2 pathway played an important role in this process.

Indexed as

Acute Lung InjuryOxidative StressPulmonary FibrosisSevofluraneAnimalsAntioxidantsApoptosisKelch-Like ECH-Associated Protein 1LipopolysaccharidesLungMiceNF-E2-Related Factor 2RAW 264.7 CellsReactive Oxygen SpeciesAntioxidantsKelch-Like ECH-Associated Protein 1LipopolysaccharidesNF-E2-Related Factor 2Reactive Oxygen SpeciesSevofluranecell apoptosislipopolysaccharideoxidative stresspulmonary fibrosisSevoflurane

Identifiers

PMID35801580
PMCPMC9272930
OpenAlexW4284886919

What Socratic 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 Socratic graph.