Evidence map›Paper›PMID 27083155›Full record

ArticleNeurotoxicity research2016

Carnosic Acid Affords Mitochondrial Protection in Chlorpyrifos-Treated Sh-Sy5y Cells.

Marcos Roberto de Oliveira, Alessandra Peres, Gustavo Costa Ferreira, Patrícia Fernanda Schuck, Simone Morelo Dal Bosco

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
7.1field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

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  16. α-Cyperone Attenuates HFrontiers in pharmacology · 2020
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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

5 authors at 5 institutions in 1 country.

Marcos Roberto de OliveiraDepartment of Chemistry/ICET, Federal University of Mato Grosso (UFMT), Av. Fernando Corrêa da Costa, 2367, Cuiaba, MT, CEP 78060-900, Brazil. mrobioq@yahoo.com.br.
Alessandra PeresHealth Basic Sciences Department, Federal University of Health Sciences of Porto Alegre, RS, Brazil.
Gustavo Costa FerreiraInstituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Patrícia Fernanda SchuckLaboratório de Erros Inatos do Metabolismo, Unidade Acadêmica de Ciências da Saúde, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense (UNESC), Criciúma, SC, Brazil.
Simone Morelo Dal BoscoFederal University of Health Sciences of Porto Alegre, Porto Alegre, RS, Brazil.
Centro Universitário Metodista IPA · BRUniversidade do Extremo Sul Catarinense · BRUniversidade Federal de Ciências da Saúde de Porto Alegre · BRUniversidade Federal de Mato Grosso · BRUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carnosic acid (CA; C20H28O4) is a phenolic diterpene found in rosemary (Rosmarinus officinalis L.) and exhibits protective properties, e.g., antioxidant, anti-inflammatory, antitumor, and antimicrobial activities. In this context, CA has been viewed as a neuroprotective agent due to its ability in rescuing neuronal cells from pro-oxidant and pro-apoptotic challenges. In the present work, we found that CA pretreatment at 1 µM for 12 h suppressed the mitochondria-related pro-oxidant and mitochondria-dependent pro-apoptotic effects of chlorpyrifos (CPF) in human neuroblastoma SH-SY5Y cells. CA prevented mitochondrial membrane potential disruption and decreased the levels of oxidative stress markers in mitochondrial membranes obtained from cells exposed to CPF. CA also inhibited cytochrome c release and activation of the caspases-9 and -3, as well as decreased DNA fragmentation, in CPF-treated cells. CA upregulated the content of glutathione (GSH) in mitochondria by a mechanism involving the activation of the phosphoinositide-3-kinase (PI3K)/Akt/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, since inhibition of PI3K/Akt or silencing of Nrf2 using siRNA strategy abolished the protection exerted by CA in SH-SY5Y cells. Therefore, CA protected mitochondria of SH-SY5Y cells through the activation of the PI3K/Akt/Nrf2 axis, causing upregulation of the mitochondrial GSH content and consequent antioxidant and anti-apoptotic effects.

Indexed as

AbietanesAntioxidantsApoptosisCaspase 3Caspase 9Cell Line, TumorCell SurvivalChlorpyrifosCytochromes cDNA FragmentationDrug Evaluation, PreclinicalGlutathioneHumansMembrane Potential, MitochondrialMitochondriaNeuroprotective AgentsAbietanesAntioxidantsCASP3 protein, humanCASP9 protein, humanCaspase 3Caspase 9ChlorpyrifosCytochromes cGlutathioneNeuroprotective AgentsNFE2L2 protein, humanNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRNA, Small InterferingsalvinAntioxidantCarnosic acidChlorpyrifosMitochondriaNrf2

Identifiers

PMID27083155
OpenAlexW2341000748

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.