Evidence map›Paper›PMID 33083022›Full record

ArticleCell death discovery2020

Cannabinoid CB1 receptor agonist ACEA alleviates brain ischemia/reperfusion injury via CB1-Drp1 pathway.

Shuai Yang, Bin Hu, Zongming Wang, Changming Zhang, Haosen Jiao, Zhigang Mao, Liguang Wei, Ji Jia, Jingling Zhao

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 34 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

9 authors at 4 institutions in 1 country.

Shuai Yang *Department of Neurosurgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Bin Hu *Department of Neurosurgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Zongming WangDepartment of Neurosurgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Changming ZhangDepartment of Neurosurgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Haosen JiaoDepartment of Neurosurgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Zhigang MaoDepartment of Neurosurgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Liguang WeiDepartment of Neurosurgery, The Second People's Hospital of Qinzhou City, Qinzhou, China.
Ji JiaDepartment of Anesthesiology, General Hospital of Southern Theatre Command of PLA, Guangzhou, China.
Jingling ZhaoDepartment of Burns, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNQinhuangdao Second Hospital · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81701908
6 · The paper itself

Abstract

Activation of the cannabinoid CB1 receptor induces neuroprotection against brain ischemia/reperfusion injury (IRI); however, the mechanism is still unknown. In this study, we used oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in neuronal cells and middle cerebral artery occlusion (MCAO)-induced brain IRI in rats to mimic ischemic brain injury, and hypothesized that the CB1 receptor agonist arachidonyl-2-chloroethylamide (ACEA) would protect ischemic neurons by inhibiting mitochondrial fission via dynamin-related protein 1 (Drp1). We found that OGD/R injury reduced cell viability and mitochondrial function, increased lactate dehydrogenase (LDH) release, and increased cell apoptosis, and mitochondrial fission. Notably, ACEA significantly abolished the OGD/R-induced neuronal injuries described above. Similarly, ACEA significantly reversed MCAO-induced increases in brain infarct volume, neuronal apoptosis and mitochondrial fission, leading to the recovery of neurological functions. The neuroprotective effects of ACEA were obviously blocked by coadministration of the CB1 receptor antagonist AM251 or by the upregulation of Drp1 expression, indicating that ACEA alleviates brain IRI via the CB1-Drp1 pathway. Our findings suggest that the CB1 receptor links aberrant mitochondrial fission to brain IRI, providing a new therapeutic target for brain IRI treatment.

Indexed as

Cell deathNeurological disorders

Identifiers

PMID33083022
PMCPMC7548964
OpenAlexW3093154991

What OpenQuestion holds

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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.