Evidence map›Paper›PMID 36756709›Full record

ArticleCNS neuroscience & therapeutics2023

Dl-3-n-butylphthalide promotes synaptic plasticity by activating the Akt/ERK signaling pathway and reduces the blood-brain barrier leakage by inhibiting the HIF-1α/MMP signaling pathway in vascular dementia model mice.

Ping Che, Juan Zhang, Mingqian Yu, Ping Tang, Yanhui Wang, Aolei Lin, Jing Xu, Nan Zhang

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. A review of animal models of vascular dementia.Molecular biology reports · 2026
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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

8 authors at 3 institutions in 1 country.

Ping CheDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Juan ZhangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Mingqian YuSchool of Medicine, Nankai University, Tianjin, China.
Ping TangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Yanhui WangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Aolei LinDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Jing XuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Nan ZhangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.ORCID 0000-0002-9675-5322
Tianjin Medical University General Hospital · CNHengshui University · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsDL-3-n-butylphthalide (NBP) exerts beneficial effects on global cognitive functions, but the underlying molecular mechanisms are still poorly understood. The present study aimed to investigate whether NBP mediates synaptic plasticity and blood-brain barrier (BBB) function, which play a pivotal role in the pathogenesis of vascular dementia (VaD), in a mouse model of bilateral common carotid artery stenosis (BCAS).

methodsNBP was administered to model mice at a dose of 80 mg/kg by gavage for 28 days after surgery. Cognitive function was evaluated by behavioral tests, and hippocampal synaptic plasticity was evaluated by in vivo electrophysiological recording. Cerebral blood flow (CBF), hippocampal volume, and white matter integrity were measured with laser speckle imaging (LSI) and MRI. In addition, BBB leakage and the expression of proteins related to the Akt/ERK and HIF-1α/MMP signaling pathways were assessed by biochemical assays.

resultsNBP treatment alleviated cognitive impairment, hippocampal atrophy, and synaptic plasticity impairment induced by BCAS. In addition, NBP treatment increased CBF, promoted white matter integrity, and decreased BBB leakage. Regarding the molecular mechanisms, in mice  with BCAS, NBP may activate the Akt/ERK signaling pathway, which upregulates the expression of synapse-associated proteins, and it may also inhibit the HIF-1α/MMP signaling pathway, thereby increasing the expression of tight junction (TJ) proteins.

conclusionIn conclusion, our results demonstrated the therapeutic effects of NBP in improving cognitive function via a wide range of targets in mice subjected to BCAS.

Indexed as

Blood-Brain BarrierDementia, VascularAnimalsBenzofuransMiceNeuronal PlasticityProto-Oncogene Proteins c-aktSignal Transduction3-n-butylphthalideBenzofuransProto-Oncogene Proteins c-aktbilateral common carotid artery stenosisblood-brain barrierDL-3-n-butylphthalidesynaptic plasticityvascular dementia

Identifiers

PMID36756709
PMCPMC10068471
OpenAlexW4319656857

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.