Evidence map›Paper›PMID 26086415›Full record

ArticleScientific reports2015

Isoflurane preconditioning provides neuroprotection against stroke by regulating the expression of the TLR4 signalling pathway to alleviate microglial activation.

Meiyan Sun, Bin Deng, Xiaoyong Zhao, Changjun Gao, Lu Yang, Hui Zhao, Daihua Yu, Feng Zhang, Lixian Xu, Lei Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
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  14. The Role of Circular RNAs in Ischemic Stroke.Neurochemical research · 2023
    Review
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2 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Meiyan SunDepartment of Anesthesiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
Bin DengDepartment of Anesthesiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
Xiaoyong ZhaoDepartment of Anesthesiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
Changjun GaoDepartment of Anesthesiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
Lu YangDepartment of Anesthesiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
Hui ZhaoDepartment of Anesthesiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
Daihua YuDepartment of Anesthesiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
Feng ZhangDepartment of Medical Administration, Lintong Sanatorium of PLA Lanzhou Military District, Lintong, Xi'an, 710600, China.
Lixian XuState Key Laboratory of Military Stomatology, Department of Anesthesiology, School of Stomatology, Fourth Military Medical University, Xi'an 710032, China.
Lei ChenDepartment of Gynaecology and Obstetrics, Nave General Hospital, Beijing, 100059, China.
Xude SunDepartment of Anesthesiology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
Air Force Medical University · CNPLA Navy General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive microglial activation often contributes to inflammation-mediated neurotoxicity in the ischemic penumbra during the acute stage of ischemic stroke. Toll-like receptor 4 (TLR4) has been reported to induce microglial activation via the NF-κB pathway. Isoflurane preconditioning (IP) can provide neuroprotection and inhibit microglial activation. In this study, we investigated the roles of the TLR4 signalling pathway in IP to exert neuroprotection following ischemic stroke in vivo and in vitro. The results showed that 2% IP alleviated neurological deficits, reduced the infarct volume, attenuated apoptosis and weakened microglial activation in the ischemic penumbra. Furthermore, IP down-regulated the expression of HSP 60, TLR4 and MyD88 and up-regulated inhibitor of IκB-α expression compared with I/R group in vivo. In vitro, 2% IP and a specific inhibitor of TLR4, CLI-095, down-regulated the expression of TLR4, MyD88, IL-1β, TNF-α and Bax, and up-regulated IκB-α and Bcl-2 expression compared with OGD group. Moreover, IP and CLI-095 attenuated microglial activation-induced neuronal apoptosis, and overexpression of the TLR4 gene reversed the neuroprotective effects of IP. In conclusion, IP provided neuroprotection by regulating TLR4 expression directly, alleviating microglial activation and neuroinflammation. Thus, inhibiting the activation of microglial activation via TLR4 may be a new avenue for stroke treatment.

Indexed as

AnimalsApoptosisBiomarkersBrain InfarctionCells, CulturedChaperonin 60Disease Models, AnimalGene ExpressionGene Expression RegulationI-kappa B ProteinsIschemic PreconditioningIsofluraneMaleMicrogliaModels, MolecularMyeloid Differentiation Factor 88BiomarkersChaperonin 60I-kappa B ProteinsIsofluraneMyeloid Differentiation Factor 88Neuroprotective AgentsNF-KappaB Inhibitor alphaNfkbia protein, ratToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID26086415
PMCPMC4471883
OpenAlexW2410317808

What OpenQuestion holds

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LicenceCC BY
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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.