Evidence map›Paper›PMID 31654382›Full record

ArticleNeurotoxicity research2020

A Synthetic Snake-Venom-Based Tripeptide Protects PC12 Cells from the Neurotoxicity of Acrolein by Improving Axonal Plasticity and Bioenergetics.

Carolina P Bernardes, Neife A G Santos, Tassia R Costa, Flavia Sisti, Lilian Amaral, Danilo L Menaldo, Martin K Amstalden, Diego L Ribeiro, Lusânia M G Antunes, Suely Vilela Sampaio and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Activation of M1 muscarinic acetylcholine receptors by proline-rich oligopeptide 7a (<EDGPIPP) fromThe journal of venomous animals and toxins including tropical diseases · 2024
    Article
  2. Article
  3. Acrolein exerts a genotoxic effect in the Leydig cells by stimulating DNA damage-induced apoptosis.Environmental science and pollution research international · 2020
    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

11 authors.

Carolina P BernardesDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Neife A G SantosDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Tassia R CostaDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Flavia SistiDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Lilian AmaralDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Danilo L MenaldoDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Martin K AmstaldenDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Diego L RibeiroDepartment of Genetics, Ribeirão Preto Medical School, University of São Paulo, Avenida Bandeirantes, 3900,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Lusânia M G AntunesDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Suely Vilela SampaioDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil.
Antonio C SantosDepartment of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Avenida do Café s/n,, Ribeirão Preto, São Paulo, 14049-900, Brazil. acsantos@fcfrp.usp.br.ORCID http://orcid.org/0000-0001-9016-2027

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior code 001Fundação de Amparo à Pesquisa do Estado de São Paulo 2011/23236-4Fundação de Amparo à Pesquisa do Estado de São Paulo 2015/24808-2
6 · The paper itself

Abstract

The synthetic peptide p-BTX-I is based on the native peptide (formed by glutamic acid, valine and tryptophan) isolated from Bothrops atrox venom. We have previously demonstrated its neuroprotective and neurotrophic properties in PC12 cells treated with the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP+). Now, we have investigated the neuroprotective effects and mechanisms of p-BTX-I against the toxicity of acrolein in PC12 cells. Studies have demonstrated that acrolein might play an important role in the etiology of Alzheimer's disease (AD), which is characterized by neuronal and synaptic loss. Our results showed that not only acrolein reduced cell differentiation and cell viability, but also altered the expression of markers of synaptic communication (synapsin I), energy metabolism (AMPK-α, Sirt I and glucose uptake), and cytoskeleton (β-III-tubulin). Treatment with p-BTX-I increased the percentage of differentiation in cells treated with acrolein and significantly attenuated cell viability loss, besides counteracting the negative effects of acrolein on synapsin I, AMPK-α, Sirt I, glucose uptake, and β-III-tubulin. Additionally, p-BTX-I alone increased the expression of apolipoprotein E (apoE) gene, associated with the proteolytic degradation of β-amyloid peptide aggregates, a hallmark of AD. Taken together, these findings demonstrate that p-BTX-I protects against acrolein-induced neurotoxicity and might be a tool for the development of novel drugs for the treatment of neurodegenerative diseases.

Indexed as

AcroleinAMP-Activated Protein KinasesAnimalsApolipoproteins EBiomarkersCell DifferentiationCell SurvivalEnergy MetabolismGlucoseNeuronal PlasticityNeuroprotective AgentsPC12 CellsPeptidesRatsSirtuin 1SynapsinsAcroleinAMP-Activated Protein KinasesApolipoproteins EBiomarkersGlucoseNeuroprotective AgentsPeptidesPrkaa1 protein, ratSirtuin 1SynapsinsTubulinAcroleinAxonal regenerationNeurodegenerationNeuroprotectionP-BTX-ISnake-venom peptides

Identifiers

PMID31654382

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.