Evidence map›Paper›PMID 34687331›Full record

ArticleExperimental brain research2022

The neuroprotection of hyperbaric oxygen therapy against traumatic brain injury via NF-κB/MAPKs-CXCL1 signaling pathways.

Anqi Xia, Huan Huang, Wenjun You, Ying Liu, Hongqin Wu, Su Liu

Abstract read
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In one paragraph

Article in Experimental brain research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.7field-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

20 citing papers in PubMed, 55 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

6 authors at 1 institution in 1 country.

Anqi Xia *Department of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Huan Huang *Department of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Wenjun You *Department of Geriatrics, the Second Peoples Hospital of Nantong, Affiliated of Nantong University, Nantong, 226001, Jiangsu, China.
Ying LiuDepartment of Pathology, Affiliated Hospital of Nantong University, Nantong, China.
Hongqin WuDepartment of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Su LiuDepartment of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China. 327202278@qq.com.ORCID http://orcid.org/0000-0002-4234-4368
Nantong University · CN

Funding

national natural science foundation of china No. 81702223science and technology planning project of nantong MS22019006
6 · The paper itself

Abstract

It is well known that hyperbaric oxygen (HBO) therapy achieves neuroprotective effects by modulating neuroinflammatory responses. However, its underlying therapeutic mechanisms are not yet fully elucidated. Based on our previous studies, we further investigated whether HBO therapy exerts neuroprotective effects in vivo by regulating the nuclear factor-kappa B (NF-κB)/ mitogen-activated protein kinases (MAPKs) chemokine (C-X-C motif) ligand (CXCL)1 inflammatory pathway. In our study, a rat model of traumatic brain injury (TBI) was established by controlled cortical impact (CCI) to verify that the expression of CXCL1 and chemokine (C-X-C motif) receptor (CXCR)2 increased after TBI, and CXCL1 was mainly expressed in astrocytes, while CXCR2 was mainly expressed in neurons. Increased apoptosis of cortical nerve cells in the injured cortex was also found after TBI. Reduced nerve cell apoptosis with improved neurological function was observed after application of a CXCR2 antagonist. The expression of phospho-extracellular signal-regulated kinase (p-ERK), phospho-c-Jun N-terminal kinase (p-JNK) and p-NF-κB increased after TBI, and application of ERK, JNK and NF-κB inhibitors decreased expression of CXCL1 and CXCR2 in rats. We further found that HBO therapy down-regulated the expression of p-ERK, p-JNK, p-NF-κB, CXCL1, and CXCR2, and reduced nerve cell apoptosis, improved the neurological function of TBI rats, and ultimately alleviated the secondary injury. In conclusion, HBO therapy may exert neuroprotective effect by regulating the NF-κB/MAPKs (JNK and ERK)-CXCL1 inflammatory pathways following TBI, which probably provide the theoretical and experimental basis for the clinical application of HBO therapy in the treatment of TBI.

Indexed as

Brain Injuries, TraumaticHyperbaric OxygenationAnimalsChemokine CXCL1MAP Kinase Signaling SystemNeuroprotectionNF-kappa BRatsRats, Sprague-DawleyChemokine CXCL1Cxcl1 protein, ratNF-kappa BCXCL1CXCR2Hyperbaric oxygenTraumatic brain injury

Identifiers

PMID34687331
OpenAlexW3114315600

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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.