Evidence map›Paper›PMID 31776590›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2020

Isoespintanol, a monoterpene isolated from oxandra cf xylopioides, ameliorates the myocardial ischemia-reperfusion injury by AKT/PKCε/eNOS-dependent pathways.

Luisa F González Arbeláez, Alejandro Ciocci Pardo, Juliana C Fantinelli, Benjamín Rojano, Guillermo R Schinella, Susana M Mosca

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Isoespintanol Isolated fromPlants (Basel, Switzerland) · 2025
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  10. Cryoprotective Effects of Ergothioneine and Isoespintanol on Canine Semen.Animals : an open access journal from MDPI · 2021
    Article
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

6 authors at 3 institutions in 2 countries.

Luisa F González ArbeláezCentro de Investigaciones Cardiovasculares ¨Dr Horacio E. Cingolani¨, CCT-CONICET, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 60 y 120, 1900, La Plata, Argentina.
Alejandro Ciocci PardoCentro de Investigaciones Cardiovasculares ¨Dr Horacio E. Cingolani¨, CCT-CONICET, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 60 y 120, 1900, La Plata, Argentina.
Juliana C FantinelliCentro de Investigaciones Cardiovasculares ¨Dr Horacio E. Cingolani¨, CCT-CONICET, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 60 y 120, 1900, La Plata, Argentina.
Benjamín RojanoLaboratorio de Ciencias de los Alimentos, Facultad de Ciencias, Universidad Nacional de Colombia (sede Medellín), Bogotá, Colombia.
Guillermo R SchinellaFacultad de Ciencias Médicas, Universidad Nacional de La Plata CIC-PBA, La Plata, Argentina.
Susana M MoscaCentro de Investigaciones Cardiovasculares ¨Dr Horacio E. Cingolani¨, CCT-CONICET, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 60 y 120, 1900, La Plata, Argentina. smosca@med.unlp.edu.ar.
Universidad Nacional de La Plata · ARConsejo Nacional de Investigaciones Científicas y Técnicas · ARUniversidad Nacional de Colombia · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo determine the actions of isoespintanol (Isoesp) on post-ischemic myocardial and mitochondrial alterations.

methodsHearts removed from Wistar rats were perfused by 20 min. After this period, the coronary flow was interrupted by half an hour and re-established during 1 h. In the treated group, Isoesp was administered at the beginning of reperfusion. To assess the participation of ε isoform of protein kinase C (PKCε), protein kinase B (PKB/Akt), and nitric oxide synthase (NOS), hearts were treated with Isoesp plus the respective inhibitors (chelerythrine, wortmannin, and N-nitro-L-arginine methyl ester). Cell death was determined by triphenyl tetrazolium chloride staining technique. Post-ischemic recovery of contractility, oxidative stress, and content of phosphorylated forms of PKCε, Akt, and eNOS were also examined. Mitochondrial state was assessed through the measurement of calcium-mediated response, calcium retention capacity, and mitochondrial potential.

resultsIsoesp limited cell death, decreased post-ischemic dysfunction and oxidative stress, improved mitochondrial state, and increased the expression of PKCε, Akt, and eNOS phosphorylated. All these beneficial effects achieved by Isoesp were annulled by the inhibitors.

conclusionThese findings suggest that activation of Akt/eNOS and PKCε signaling pathways are involved in the development of Isoesp-induced cardiac and mitochondria tolerance to ischemia-reperfusion.

Indexed as

AnimalsAnnonaceaeCardiotonic AgentsHeartIn Vitro TechniquesMaleMitochondria, HeartMonoterpenesMyocardial ContractionMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumNitric Oxide Synthase Type IIIProtein Kinase C-epsilonProto-Oncogene Proteins c-aktRats, WistarCardiotonic AgentsisoespintanolMonoterpenesNitric Oxide Synthase Type IIINos3 protein, ratProtein Kinase C-epsilonProto-Oncogene Proteins c-aktAkteNOSInfarct sizeIschemia-reperfusionIsoespintanolPKCε

Identifiers

PMID31776590
OpenAlexW2991466552

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.