Evidence map›Paper›PMID 31867811›Full record

ArticleInternational journal of experimental pathology2019

Resveratrol attenuates cerebral ischaemia reperfusion injury via modulating mitochondrial dynamics homeostasis and activating AMPK-Mfn1 pathway.

Jinbao Gao, Haijiang Wang, Yunjun Li, Wende Li

Abstract read
In one paragraph

Article in International journal of experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

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  8. A detailed review of pharmacology of MFN1 (mitofusion-1)-mediated mitochondrial dynamics: Implications for cellular health and diseases.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
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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

4 authors.

Jinbao GaoDepartment of Neurosurgery, the Seventh Medical Center, the PLA Army General Hospital, Beijing, China.
Haijiang WangDepartment of Neurosurgery, the Seventh Medical Center, the PLA Army General Hospital, Beijing, China.
Yunjun LiDepartment of Neurosurgery, the Seventh Medical Center, the PLA Army General Hospital, Beijing, China.ORCID 0000-0002-8606-0711
Wende LiDepartment of Neurosurgery, the Seventh Medical Center, the PLA Army General Hospital, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of cerebral ischaemia reperfusion injury (IRI) has not been fully described. Accordingly, there is little effective drug available for the treatment of cerebral IRI. The aim of our study was to explore the exact role played by Mfn1-mediated mitochondrial protection in cerebral IRI and evaluate the beneficial action of resveratrol on reperfused brain. Our study demonstrated that hypoxia-reoxygenation (HR) injury caused N2a cell apoptosis and this process was highly affected by mitochondrial dysfunction. Decreased mitochondrial membrane potential, increased mitochondrial oxidative stress, and an activated mitochondrial apoptosis pathway were noted in HR-treated N2a cells. Interestingly, resveratrol treatment could attenuate N2a cell apoptosis via sustaining mitochondrial homeostasis. Further, we found that resveratrol modulated mitochondrial performance via activating the Mfn1-related mitochondrial protective system. Knockdown of Mfn1 could abolish the beneficial effects of resveratrol on HR-treated N2a cells. Besides, we also report that resveratrol regulated Mfn1 expression via the AMPK pathway; inhibition of AMPK pathway also neutralized the anti-apoptotic effect of resveratrol on N2a cells in the setting of cerebral IRI. Taken together our results show that mitochondrial damage is closely associated with the progression of cerebral IRI. In addition we also demonstrate the protective action played by resveratrol on reperfused brain and show that this effect is achieved via activating the AMPK-Mfn1 pathway.

Indexed as

AMP-Activated Protein KinasesAnimalsBrainCell LineGTP PhosphohydrolasesHomeostasisMiceMitochondriaMitochondrial DynamicsNeuroprotective AgentsReperfusion InjuryResveratrolSignal TransductionAMP-Activated Protein KinasesGTP PhosphohydrolasesMfn1 protein, mouseNeuroprotective AgentsResveratrolAMPK pathwaycerebral IR injuryMfn1mitochondrial stressresveratrol

Identifiers

PMID31867811
PMCPMC7042761

What OpenQuestion holds

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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.