Evidence map›Paper›PMID 28591721›Full record

ArticleOncotarget2017

Ginkgolide K attenuates neuronal injury after ischemic stroke by inhibiting mitochondrial fission and GSK-3β-dependent increases in mitochondrial membrane permeability.

Xu Zhou, Hui-Ying Wang, Bin Wu, Cai-Yi Cheng, Wei Xiao, Zhen-Zhong Wang, Yu-Yu Yang, Ping Li, Hua Yang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed, 84 citations in OpenAlex.

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  19. Piceatannol protects rat neuron cells from oxygen-glucose deprivation reperfusion injury via regulation of GSK-3β/Nrf2 signaling pathway.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Article
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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

9 authors at 2 institutions in 1 country.

Xu ZhouState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Hui-Ying WangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Bin WuState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Cai-Yi ChengState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Wei XiaoState Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Jiangsu Kanion Pharmaceutical Co., Ltd., Lianyungang, China.
Zhen-Zhong WangState Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Jiangsu Kanion Pharmaceutical Co., Ltd., Lianyungang, China.
Yu-Yu YangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Ping LiState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Hua YangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
China Pharmaceutical University · CNKanion Pharmaceutical (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ginkgolide K (GK) belongs to the ginkgolide family of natural compounds found in Ginkgo biloba leaves, which have been used for centuries to treat cerebrovascular and cardiovascular diseases. We evaluated the protective effects of GK against neuronal apoptosis by assessing its ability to sustain mitochondrial integrity and function. Co-immunoprecipitation showed that Drp1 binding to GSK-3β was increased after an oxygen-glucose deprivation/reperfusion (OGD/R) insult in cultured neuroblastoma cells. This induced Drp1 and GSK-3β translocation to mitochondria and mitochondrial dysfunction, which was attenuated by GK. GK also reduced mitochondrial fission by increasing Drp1 phosphorylation at Ser637 and inhibiting mitochondrial Drp1 recruitment. In addition, GK exposure induced GSK-3β phosphorylation at Ser9 and enhanced the interaction between adenine nucleotide translocator (ANT) and p-GSK-3β. This interaction suppressed the interaction between ANT and cyclophilin D (CypD), which inhibited mitochondrial permeability transition pore (mPTP) opening. Similarly, suppression of mitochondrial fission by Mdivi-1 also inhibited GSK-3β-induced mPTP opening. Treating mice with GK prevented GSK-3β and Drp1 translocation to mitochondria and attenuated mitochondrial dysfunction after middle cerebral artery occlusion. We therefore propose that by inhibiting mitochondrial fission and attenuating mPTP opening, GK exerts neuroprotective effects that mitigate or prevent neuronal damage secondary to ischemic stroke.

Indexed as

AnimalsApoptosisBrain IschemiaCell LineCytochromes cDynaminsGinkgolidesGlucoseGlycogen Synthase Kinase 3 betaIon Channel GatingLactonesMaleMiceMitochondrial DynamicsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreCytochromes cDnm1l protein, mouseDynaminsginkgolide KGinkgolidesGlucoseGlycogen Synthase Kinase 3 betaLactonesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNeuroprotective AgentsOxygenReactive Oxygen Speciesginkgolide Kischemic strokemitochondrial fissionmitochondrial permeability transition poreneuron apoptosis

Identifiers

PMID28591721
PMCPMC5546510
OpenAlexW2615253431

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.