Evidence map›Paper›PMID 29113305›Full record

ArticleOncotarget2017

Vinpocetine alleviate cerebral ischemia/reperfusion injury by down-regulating TLR4/MyD88/NF-κB signaling.

Li-Rong Wu, Liang Liu, Xiao-Yi Xiong, Qin Zhang, Fa-Xiang Wang, Chang-Xiong Gong, Qi Zhong, Yuan-Rui Yang, Zhao-You Meng, Qing-Wu Yang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

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  14. Remote ischemic conditioning enhances oxygen supply to ischemic brain tissue in a mouse model of stroke: Role of elevated 2,3-biphosphoglycerate in erythrocytes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 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

10 authors at 1 institution in 1 country.

Li-Rong WuDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Liang LiuDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Xiao-Yi XiongDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Qin ZhangDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Fa-Xiang WangDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Chang-Xiong GongDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Qi ZhongDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Yuan-Rui YangDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Zhao-You MengDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Qing-Wu YangDepartment of Neurology, Xinqiao Hospital, The Third Military Medical University, Shapingba, Chongqing, China.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory responses play crucial roles in cerebral ischemia/reperfusion injury. Toll-like receptor 4 (TLR4) is an important mediator of the neuroinflammatory response to cerebral ischemia/reperfusion injury. Vinpocetine is a derivative of the alkaloid vincamine and exerts an anti-inflammatory effect by inhibiting NF-κB activation. However, the effects of vinpocetine on pathways upstream of NF-κB signaling, such as TLR4, have not been fully elucidated. Here, we used mouse middle cerebral artery occlusion (MCAO) and cell-based oxygen-glucose deprivation (OGD) models to evaluate the therapeutic effects and mechanisms of vinpocetine treatment. The vinpocetine treatment significantly reduced mice cerebral infarct volumes and neurological scores. Moreover, the numbers of TUNEL+ and Fluoro-Jade B+ cells were significantly decreased in the ischemic brain tissues after vinpocetine treatment. In the OGD model, the vinpocetine treatment also increased the viability of cultured cortical neurons. Interestingly, vinpocetine exerted a neuroprotective effect on the mouse MCAO model and cell-based OGD model by inhibiting TLR4-mediated inflammatory responses and decreasing proinflammatory cytokine release through the MyD88-dependent signaling pathway, independent of TRIF signaling pathway. In conclusion, vinpocetine exerts anti-inflammatory effects to ameliorate cerebral ischemia/reperfusion injury in vitro and in vivo. Vinpocetine may inhibit inflammatory responses through the TLR4/MyD88/NF-κB signaling pathway, independent of TRIF-mediated inflammatory responses. Thus, vinpocetine may be an attractive therapeutic candidate for the treatment of ischemic cerebral injury or other inflammatory diseases.

Indexed as

cerebral ischemia/reperfusionischemic strokemiddle cerebral artery occlusiontoll-like receptor 4vinpocetine

Identifiers

PMID29113305
PMCPMC5655200
OpenAlexW2752917280

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.