Evidence map›Paper›PMID 29904091›Full record

ArticleActa pharmacologica Sinica2019

Naloxone attenuates ischemic brain injury in rats through suppressing the NIK/IKKα/NF-κB and neuronal apoptotic pathways.

Xuan Wang, Zu-Jun Sun, Jun-Lu Wu, Wen-Qiang Quan, Wei-Dong Xiao, Helen Chew, Cui-Min Jiang, Dong Li

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2019. 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
1.4field-weighted citation impact, top 18% 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, 24 citations in OpenAlex.

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  16. IpsilesionalBrain communications · 2020
    Article
  17. Neuroprotective Peptides in Retinal Disease.Journal of clinical medicine · 2019
    Review
  18. Article
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

8 authors at 4 institutions in 2 countries.

Xuan WangDepartment of Pharmacy, Putuo People's Hospital, Shanghai, 200060, China.
Zu-Jun SunDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Jun-Lu WuDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Wen-Qiang QuanDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Wei-Dong XiaoSol Sherry Thrombosis Research Center, Temple University, Philadelphia, PA, 19140, USA.
Helen ChewSol Sherry Thrombosis Research Center, Temple University, Philadelphia, PA, 19140, USA.
Cui-Min JiangDepartment of Pharmacy, Putuo People's Hospital, Shanghai, 200060, China. 1098618044@qq.com.
Dong LiDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China. lidong@tongji.edu.cn.
Central Hospital of Putuo District · CNTemple University · USTongji Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although naloxone has been documented to exert neuroprotection in animal model of cerebral ischemia, the mechanism is not well understood. In this present study we investigated whether naloxone affected the mitochondrial apoptotic pathway in ischemic brain injury of rats. SD rats were subjected to a permanent middle cerebral artery occlusion surgery, and received naloxone (0.5, 1, 2 mg/kg, i.v.) immediately after ischemia. Neurological deficits were evaluated 24 h after ischemia using the McGraw Stroke Index, and then the rats were killed, and the brains were collected for further analyses. We show that naloxone treatment dose-dependently decreased the infarction volume and morphological injury, improved motor behavioral function, and markedly curtailed brain edema. Furthermore, naloxone administration significantly inhibited the nuclear translocation of NF-κB p65 and decreased the levels of nuclear NF-κB p65 in the ischemic penumbra. Naloxone administration also dose-dependently increased the NF-κB inhibitory protein (IκBα) levels and attenuated phosphorylated NIK and IKKα levels in the ischemic penumbra. In addition, naloxone administration dose-dependently increased Bcl-2 levels, decreased Bax levels, stabilized the mitochondrial transmembrane potential, and inhibited cytochrome c release and caspase 3 and caspase 9 activation. These results indicate that the neuroprotective effects of naloxone against ischemic brain injury involve the inhibition of NF-κB activation via the suppression of the NIK/IKKα/IκBα pathway and the obstruction of the mitochondrial apoptotic pathway in neurons.

Indexed as

AnimalsApoptosisI-kappa B KinaseInfarction, Middle Cerebral ArteryMaleMitochondriaNaloxoneNeuroprotective AgentsNF-kappa BNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesRats, Sprague-DawleySignal TransductionI-kappa B KinaseNaloxoneNeuroprotective AgentsNF-kappa BNF-kappaB-Inducing KinaseProtein Serine-Threonine Kinasescerebral ischemiamitochondrial apoptotic pathwaynaloxoneneuroprotectionNF-κB

Identifiers

PMID29904091
PMCPMC6329773
OpenAlexW2808500918

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.