Evidence map›Paper›PMID 34018697›Full record

ArticleCNS neuroscience & therapeutics2021

Naltrexone is neuroprotective against traumatic brain injury in mu opioid receptor knockout mice.

Yu-Syuan Wang, Tsai-Wei Hung, Eun-Kyung Bae, Kuo-Jen Wu, Wei Hsieh, Seong-Jin Yu

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Recent progresses in novelFrontiers in bioengineering and biotechnology · 2022
    Review
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.

Yu-Syuan WangCenter for Neuropsychiatric Research, National Health Research Institute, Zhunan, Taiwan.
Tsai-Wei HungCenter for Neuropsychiatric Research, National Health Research Institute, Zhunan, Taiwan.
Eun-Kyung BaeCenter for Neuropsychiatric Research, National Health Research Institute, Zhunan, Taiwan.
Kuo-Jen WuCenter for Neuropsychiatric Research, National Health Research Institute, Zhunan, Taiwan.
Wei HsiehCenter for Neuropsychiatric Research, National Health Research Institute, Zhunan, Taiwan.
Seong-Jin YuCenter for Neuropsychiatric Research, National Health Research Institute, Zhunan, Taiwan.ORCID 0000-0001-7500-5883
National Health Research Institutes · TW

Funding

National Health Research Institutes, Taiwan NP-106-PP-02National Health Research Institutes, Taiwan NP-107-PP-02The Ministry of Science and Technology, Taiwan MOST 108-2320-B-400-023
6 · The paper itself

Abstract

aimsNaltrexone is a mu opioid receptor (MOR) antagonist used to treat drug dependence in patients. Previous reports indicated that MOR antagonists reduced neurodegeneration and inflammation after brain injury. The purpose of this study was to evaluate the neuroprotective effect of naltrexone in cell culture and a mouse model of traumatic brain injury (TBI).

methodsThe neuroprotective effect of naltrexone was examined in primary cortical neurons co-cultured with BV2 microglia. Controlled cortical impact (CCI) was delivered to the left cerebral cortex of adult male MOR wild-type (WT) and knockout (KO) mice. Naltrexone was given daily for 4 days, starting from day 2 after lesioning. Locomotor activity was evaluated on day 5 after the CCI. Brain tissues were collected for immunostaining, Western, and qPCR analysis.

resultsGlutamate reduced MAP2 immunoreactivity (-ir), while increased IBA1-ir in neuron/BV2 co-culture; both responses were antagonized by naltrexone. TBI significantly reduced locomotor activity and increased the expression of IBA1, iNOS, and CD4 in the lesioned cortex. Naltrexone significantly and equally antagonized the motor deficits and expression of IBA1 and iNOS in WT and KO mice. TBI-mediated CD4 protein production was attenuated by naltrexone in WT mice, but not in KO mice.

conclusionNaltrexone reduced TBI-mediated neurodegeneration and inflammation in MOR WT and KO mice. The protective effect of naltrexone involves non-MOR and MOR mechanisms.

Indexed as

AnimalsBrain Injuries, TraumaticCoculture TechniquesMaleMiceMice, KnockoutMice, TransgenicNaltrexoneNarcotic AntagonistsNeuroprotective AgentsReceptors, Opioid, muNaltrexoneNarcotic AntagonistsNeuroprotective AgentsReceptors, Opioid, muinflammationmu opioid receptornaltrexonetraumatic brain injury

Identifiers

PMID34018697
PMCPMC8193702
OpenAlexW3160487590

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.