Evidence map›Paper›PMID 32801650›Full record

ArticleDrug design, development and therapy2020

The Protective Effects of Juglanin in Cerebral Ischemia Reduce Blood-Brain Barrier Permeability via Inhibition of VEGF/VEGFR2 Signaling.

Jia Liu, Lei Chen, Xin Zhang, Lixiao Pan, Lili Jiang

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 28 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

5 authors at 2 institutions in 1 country.

Jia LiuDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, People's Republic of China.
Lei ChenDepartment of Integrated Management, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, People's Republic of China.
Xin ZhangDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, People's Republic of China.
Lixiao PanDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, People's Republic of China.
Lili JiangDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, People's Republic of China.
Affiliated Hospital of Qingdao University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIschemic brain injury due to stroke or other pathologies is a major contributor to disability and mortality worldwide. Upon the occurrence of stroke, neuronal cells undergo apoptosis due to the deprivation of oxygen and nutrients and failure of the blood-brain barrier (BBB). In the moments immediately following a stroke, widespread perfusion resulting from hyperpermeability is accompanied by an acute inflammatory response, which induces neovascularization and often permanent neurological injury. Vascular endothelial growth factor (VEGF) and its receptor VEGF receptor 2 (VEGFR2) have been targeted to suppress cerebral ischemia. Recently, natural products including flavonoids, such as juglanin, have been receiving increasing attention for their impressive physiological effects.

methodsTwenty mg/kg body weight juglanin was administrated for 3 weeks before inducing middle cerebral artery occlusion (MCAO) in mice. The animal brain infarction volume, neurological deficit score, blood-brain barrier permeability, and the expression of tight junction proteins were evaluated. Endothelial permeability and tight junction protein expression were also assessed in brain microvascular endothelial cells (HMBVECs) exposed to oxygen-glucose deprivation/reperfusion (OGD/R).

resultsJuglanin significantly reduced occlusion-induced infarct volume and improved neurological score by suppressing BBB hyperpermeability. Juglanin inhibited both the mRNA and protein expression of VEGF and VEGFR2 and restored the normal expression of occludin and zonula occludens-1 (ZO-1), two important tight junction proteins, in MCAO mice. Meanwhile, the results of in vitro experiments show that the protective effects of juglanin against increased BBB permeability and reduced tight junction functionality are dependent on the VEGF/VEGFR2 signaling pathway, as evidenced by the capacity of exogenous VEGF-A to abolish the effects of juglanin.

conclusionOur findings indicate a potent ability of juglanin to prevent neuronal injury resulting from cerebral ischemia by modulating the VEGF/VEGFR2 signaling pathway. Further research will help elucidate the exact mechanisms behind the protective effects of juglanin.

Indexed as

Administration, OralAnimalsBlood-Brain BarrierBrain IschemiaCells, CulturedGlycosidesHumansInfarction, Middle Cerebral ArteryKaempferolsMiceMice, Inbred C57BLPermeabilityProtective AgentsRNA, MessengerSignal TransductionVascular Endothelial Growth Factor AGlycosidesjuglaninKaempferolsKdr protein, mouseProtective AgentsRNA, MessengerVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVascular Endothelial Growth Factor Receptor-2BBB permeabilityblood–brain barriercerebral ischemiajuglaninstroketight junction proteinsVEGFVEGFR2

Identifiers

PMID32801650
PMCPMC7415453
OpenAlexW3047064628

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Registered trials

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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.