Evidence map›Paper›PMID 25426944›Full record

ArticlePloS one2014

EGb761 provides a protective effect against Aβ1-42 oligomer-induced cell damage and blood-brain barrier disruption in an in vitro bEnd.3 endothelial model.

Wen-bin Wan, Lan Cao, Lu-mei Liu, Bill Kalionis, Chuan Chen, Xian-tao Tai, Ya-ming Li, Shi-jin Xia

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 56 citations in OpenAlex.

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  10. Mild Cognitive Impairment and Mild Dementia: The Role ofPharmaceuticals (Basel, Switzerland) · 2021
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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 5 institutions in 2 countries.

Wen-bin WanDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Lan CaoState Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Lu-mei LiuGeriatrics Department of Traditional Chinese Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Bill KalionisDepartment of Perinatal Medicine Pregnancy Research Centre and University of Melbourne Department of Obstetrics and Gynaecology, Royal Women's Hospital, Parkville, VIC, Australia.
Chuan ChenShanghai Geriatric Institute of Chinese Medicine, Shanghai, China.
Xian-tao TaiSchool of Acupuncture, Massage and Rehabilitation, Yunnan University of Traditional Chinese Medicine, Kunming, China.
Ya-ming LiGeriatrics Department of Traditional Chinese Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Shi-jin XiaShanghai Institute of Geriatrics, Huadong Hospital, Fudan University, Shanghai, China.
Fudan University · CNHuadong Hospital · CNUniversity of Melbourne · AUYangPu Geriatric Hospital · CNYunnan University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of senile dementia which is characterized by abnormal amyloid beta (Aβ) accumulation and deposition in brain parenchyma and cerebral capillaries, and leads to blood-brain barrier (BBB) disruption. Despite great progress in understanding the etiology of AD, the underlying pathogenic mechanism of BBB damage is still unclear, and no effective treatment has been devised. The standard Ginkgo biloba extract EGb761 has been widely used as a potential cognitive enhancer for the treatment of AD. However, the cellular mechanism underlying the effect remain to be clarified. In this study, we employed an immortalized endothelial cell line (bEnd.3) and incubation of Aβ(1-42) oligomer, to mimic a monolayer BBB model under conditions found in the AD brain. We investigated the effect of EGb761 on BBB and found that Aβ1-42 oligomer-induced cell injury, apoptosis, and generation of intracellular reactive oxygen species (ROS), were attenuated by treatment with EGb761. Moreover, treatment of the cells with EGb761 decreased BBB permeability and increased tight junction scaffold protein levels including ZO-1, Claudin-5 and Occludin. We also found that the Aβ(1-42) oligomer-induced upregulation of the receptor for advanced glycation end-products (RAGE), which mediates Aβ cytotoxicity and plays an essential role in AD progression, was significantly decreased by treatment with EGb761. To our knowledge, we provide the first direct in vitro evidence of an effect of EGb761 on the brain endothelium exposed to Aβ(1-42) oligomer, and on the expression of tight junction (TJ) scaffold proteins and RAGE. Our results provide a new insight into a possible mechanism of action of EGb761. This study provides a rational basis for the therapeutic application of EGb761 in the treatment of AD.

Indexed as

Amyloid beta-PeptidesApoptosisBlood-Brain BarrierCell Line, TransformedClaudin-5Endothelial CellsGene ExpressionGinkgo bilobaGinkgo ExtractHumansModels, BiologicalNootropic AgentsOccludinPeptide FragmentsPlant ExtractsReactive Oxygen SpeciesAmyloid beta-Peptidesamyloid beta-protein (1-42)Claudin-5CLDN5 protein, humanGinkgo biloba extractGinkgo ExtractNootropic AgentsOccludinOCLN protein, humanPeptide FragmentsPlant ExtractsReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsReceptors, ImmunologicTJP1 protein, humanZonula Occludens-1 Protein

Identifiers

PMID25426944
PMCPMC4245095
OpenAlexW1992451616

What OpenQuestion 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 OpenQuestion graph.