Evidence map›Paper›PMID 33141426›Full record

ArticleNeurotoxicity research2021

URB597 Prevents the Short-Term Excitotoxic Cell Damage in Rat Cortical Slices: Role of Cannabinoid 1 Receptors.

Karla Chavira-Ramos, Mario Orozco-Morales, Çimen Karasu, Alexey A Tinkov, Michael Aschner, Abel Santamaría, Ana Laura Colín-González

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

4 citing papers in PubMed, 26 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

7 authors at 5 institutions in 4 countries.

Karla Chavira-RamosLaboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía, S.S.A., 14269, Mexico City, Mexico.
Mario Orozco-MoralesLaboratorio de Medicina Personalizada, Instituto Nacional de Cancerología, S.S.A., 14080, Mexico City, Mexico.
Çimen KarasuCellular Stress Response and Signal Transduction Research Laboratory, Faculty of Medicine, Department of Medical Pharmacology, Gazi University, Beşevler, 06500, Ankara, Turkey.
Alexey A TinkovIM Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia.
Michael AschnerDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, 11354, USA.
Abel SantamaríaLaboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía, S.S.A., 14269, Mexico City, Mexico. absada@yahoo.com.
Ana Laura Colín-GonzálezLaboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía, S.S.A., 14269, Mexico City, Mexico.
Instituto Nacional de Cancerología · MXInstituto Nacional de Neurología y Neurocirugía · MXAlbert Einstein College of Medicine · USGazi University · TRYaroslavl State University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endocannabinoid-based therapies constitute an emerging tool for the potential treatment of neurodegenerative disorders, requiring characterization at the experimental level. The effects of URB597, an inhibitor of the fatty acid amide hydrolase (FAAH), were tested against the quinolinic acid (QUIN)-induced early toxic effects in rat cortical slices, and compared with those effects exerted by the endocannabinoid anandamide (AEA). URB597 prevented the QUIN-induced loss of mitochondrial function/cell viability and lipid peroxidation, while reduced necrosis, and to a lesser extent, apoptosis. The protective effects of URB597 were mediated by activation of cannabinoid receptor 1 (CB1r), as evidenced by their inhibition by the selective CB1r antagonist AM281. Similar effects were observed when testing AEA against QUIN toxicity. Our findings demonstrate the neuroprotective properties of URB597 during the early stages of excitotoxic damage to cortical tissue, suggesting that these properties are mediated by FAAH inhibition, and might be linked to the protective effects of AEA, or the combination of endocannabinoids.

Indexed as

AmidohydrolasesAnimalsApoptosisBenzamidesCarbamatesCells, CulturedCerebral CortexFatty Acid Amide HydrolasesMaleMitochondriaNeuroprotective AgentsOxidative StressQuinolinic AcidRatsRats, WistarReceptor, Cannabinoid, CB1AmidohydrolasesBenzamidesCarbamatesCnr1 protein, ratcyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl esterFatty Acid Amide HydrolasesNeuroprotective AgentsQuinolinic AcidReceptor, Cannabinoid, CB1AM281AnandamideEndocannabinoid systemExcitotoxicityFatty acid amide hydrolaseURB597

Identifiers

PMID33141426
OpenAlexW3096885505

What OpenQuestion holds

Textmetadata
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.