Evidence map›Paper›PMID 35112804›Full record

ArticleCNS neuroscience & therapeutics2022

The effect of propofol on hypoxia- and TNF-α-mediated BDNF/TrkB pathway dysregulation in primary rat hippocampal neurons.

Weiping Tao, Xuesong Zhang, Juan Ding, Shijian Yu, Peiqing Ge, Jingfeng Han, Xing Luo, Wei Cui, Jiawei Chen

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2022. 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
3.1field-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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  18. The Mechanism of TNF-Oxidative medicine and cellular longevity · 2022
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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

9 authors at 3 institutions in 1 country.

Weiping TaoDepartment of Anesthesiology, Jing'an District Central Hospital of Shanghai, Shanghai, China.
Xuesong ZhangDepartment of Anesthesiology, Shanghai Public Health Clinical Center, Shanghai, China.
Juan DingDepartment of Anesthesiology, Department of Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai, China.
Shijian YuDepartment of Anesthesiology, Jing'an District Central Hospital of Shanghai, Shanghai, China.
Peiqing GeDepartment of Anesthesiology, Jing'an District Central Hospital of Shanghai, Shanghai, China.
Jingfeng HanDepartment of Anesthesiology, Jing'an District Central Hospital of Shanghai, Shanghai, China.
Xing LuoDepartment of Anesthesiology, Department of Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai, China.
Wei CuiDepartment of Anesthesiology, Jing'an District Central Hospital of Shanghai, Shanghai, China.
Jiawei ChenDepartment of Anesthesiology, Jing'an District Central Hospital of Shanghai, Shanghai, China.
Jingzhou Central Hospital · CNFudan University Shanghai Cancer Center · CNShanghai Public Health Clinical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsHypoxia and inflammation may lead to BDNF/TrkB dysregulation and neurological disorders. Propofol is an anesthetic with neuroprotective properties. We wondered whether and how propofol affected BDNF/TrkB pathway in hippocampal neurons and astrocytes.

methodsPrimary rat hippocampal neurons and astrocytes were cultured and exposed to propofol followed by hypoxia or TNF-α treatment. The expression of BDNF and the expression/truncation/phosphorylation of TrkB were measured. The underlying mechanisms were investigated.

resultsHypoxia and TNF-α reduced the expression of BDNF, which was reversed by pretreatment of 25 μM propofol in hippocampal neurons. Furthermore, hypoxia and TNF-α increased the phosphorylation of ERK and phosphorylation of CREB at Ser142, while reduced the phosphorylation of CREB at Ser133, which were all reversed by 25 μM propofol and 10 μM ERK inhibitor. In addition, hypoxia or TNF-α did not affect TrkB expression, truncation, or phosphorylation in hippocampal neurons and astrocytes. However, in hippocampal neurons, 50 μM propofol induced TrkB phosphorylation, which may be mediated by p35 expression and Cdk5 activation, as suggested by the data showing that blockade of p35 or Cdk5 expression mitigated propofol-induced TrkB phosphorylation.

conclusionsPropofol modulated BDNF/TrkB pathway in hippocampal neurons via ERK/CREB and p35/Cdk5 under the condition of hypoxia or TNF-α exposure.

Indexed as

PropofolAnimalsBrain-Derived Neurotrophic FactorCells, CulturedHippocampusHypoxiaNeuronsRatsReceptor, trkBTumor Necrosis Factor-alphaBrain-Derived Neurotrophic FactorPropofolReceptor, trkBTumor Necrosis Factor-alphaBrain-derived neurotrophic factorHippocampal neuronHypoxiaPropofolTumor necrosis factor-α

Identifiers

PMID35112804
PMCPMC8981449
OpenAlexW4210500745

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LicenceCC BY
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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.