Evidence map›Paper›PMID 31478596›Full record

ArticleAnnals of clinical and translational neurology2019

Dexmedetomidine Attenuates Neuroinflammatory-Induced Apoptosis after Traumatic Brain Injury via Nrf2 signaling pathway.

Fayin Li, Xiaodong Wang, Zhijie Zhang, Xianlong Zhang, Pengfei Gao

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-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

33 citing papers in PubMed, 53 citations in OpenAlex.

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  10. Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 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.

Fayin LiDepartment of Anesthesiology, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, 6 Beijing Road West, Huaian, 223002, Jiangsu, China.
Xiaodong WangDepartment of Neurosurgery, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, 6 Beijing Road West, Huaian, 223002, Jiangsu, China.
Zhijie ZhangDepartment of Anesthesiology, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, 6 Beijing Road West, Huaian, 223002, Jiangsu, China.
Xianlong ZhangDepartment of Anesthesiology, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, 6 Beijing Road West, Huaian, 223002, Jiangsu, China.
Pengfei GaoDepartment of Anesthesiology, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, 6 Beijing Road West, Huaian, 223002, Jiangsu, China.ORCID 0000-0002-7720-332X
Huaian First People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveDexmedetomidine (DEX) exhibits neuroprotective effects as a multifunctional neuroprotective agent in numerous neurological disorders. However, in traumatic brain injury (TBI), the molecular mechanisms of these neuroprotective effects remain unclear. The present study investigated whether DEX, which has been reported to exert protective effects against TBI, could attenuate neuroinflammatory-induced apoptosis and clarified the underlying mechanisms.

methodsA weight-drop model was established, and DEX was intraperitoneally injected 30 min after inducing TBI in rats. The water content in the brain tissue was measured. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assays were performed on histopathological tissue sections to evaluate neuronal apoptosis. Enzyme-linked immunosorbent assay and PCR were applied to detect the levels of the inflammatory factors, TNF-α, IL-1β, IL-6, and NF-κB.

resultsTBI-challenged rats exhibited significant neuronal apoptosis, which was characterized via the wet-to-dry weight ratio, neurobehavioral functions, TUNEL assay results and the levels of cleaved caspase-3, Bax upregulation and Bcl-2, which were attenuated by DEX. Western blot, immunohistochemistry, and PCR results revealed that DEX promoted Nrf2 expression and upregulated expression of the Nrf2 downstream factors, HO-1 and NQO-1. Furthermore, DEX treatment markedly prevented the downregulation of inflammatory response factors, TNF-α, IL-1β and NF-κB, and IL-6.

interpretationAdministering DEX attenuated inflammation-induced brain injury in a TBI model, potentially via the Nrf2 signaling pathway.

Indexed as

AnimalsApoptosisBrainBrain Injuries, TraumaticDexmedetomidineInflammationNeuroprotective AgentsNF-E2-Related Factor 2RatsSignal TransductionDexmedetomidineNeuroprotective AgentsNfe2l2 protein, ratNF-E2-Related Factor 2

Identifiers

PMID31478596
PMCPMC6764501
OpenAlexW2972029555

What OpenQuestion 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 OpenQuestion graph.