Evidence map›Paper›PMID 30867669›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2019

Naomaitai Ameliorated Brain Damage in Rats with Vascular Dementia by PI3K/PDK1/AKT Signaling Pathway.

Kui Huang, Lei Shen, Tieming Niu, Ying Zhao, Jiucun Fu, Yunpeng Cao

Open access · hybridAbstract read
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Kui HuangDepartment of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.ORCID 0000-0001-6411-0389
Lei ShenDepartment of Geriatric Medicine, Shenyang Red Cross hospital, Shenyang Liaoning 110000, China.
Tieming NiuDepartment of Urologic Department, Shenyang Red Cross hospital, Shenyang Liaoning 110000, China.
Ying ZhaoDepartment of Health Management, Shenyang Red Cross hospital, Shenyang Liaoning 110000, China.
Jiucun FuDepartment of Geriatric Medicine, Shenyang Red Cross hospital, Shenyang Liaoning 110000, China.
Yunpeng CaoDepartment of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.ORCID 0000-0003-3177-7173
Shenyang 242 Hospital · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsNaomaitai can improve blood perfusion and ameliorate the damage in the paraventricular white matter. This study was focused on observing the neuroprotective effect of Naomaitai on the vascular dementia of rat and exploring the action mechanism of PI3K/PDK1/AKT signaling pathway.

methodsA vascular dementia model of rats was established by permanent, bilateral common carotid artery occlusion. Rats' behavior was tested by Neurological deficit score and the Morris water maze. The pathology and apoptosis were detected through HE staining and TUNEL assay. Myelin sheath loss and nerve fiber damage were detected by LFB staining. Inflammatory factors, oxidative stress, and brain damage markers were detected through ELISA. The expression of apoptosis-related proteins and PI3K/PDK1/AKT signaling pathway related proteins were measured by western blot. The expressions of PI3K, PDK1, AKT, and MBP in paraventricular white matter cells were detected by immunofluorescence.

resultsNaomaitai treatment decreased neurological function score in rats with vascular dementia, ameliorated paraventricular white matter damage caused by long-term hypoxia, and hypoperfusion reduced the brain injury markers S-100

conclusionNaomaitai can ameliorate brain damage in rats with vascular dementia, inhibit neuronal apoptosis, and have anti-inflammatory and antioxidative stress effects, which may be regulated by the PI3K/PDK1/AKT signaling pathway.

Identifiers

PMID30867669
PMCPMC6379870
OpenAlexW2914331627

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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.