Evidence map›Paper›PMID 32524380›Full record

ArticleNeurotoxicity research2020

Simvastatin Prevents Long-Term Cognitive Deficits in Sepsis Survivor Rats by Reducing Neuroinflammation and Neurodegeneration.

Carlos Henrique Rocha Catalão, Nilton Nascimento Santos-Junior, Luís Henrique Angenendt da Costa, Anderson Oliveira Souza, Evelin Capellari Cárnio, Adriano Sebollela, Luciane Carla Alberici, Maria José Alves Rocha

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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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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  10. Neurochemical effects of sepsis on the brain.Clinical science (London, England : 1979) · 2023
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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

8 authors at 2 institutions in 1 country.

Carlos Henrique Rocha CatalãoDepartment of Neurosciences and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Nilton Nascimento Santos-JuniorDepartment of Neurosciences and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Luís Henrique Angenendt da CostaDepartment of Neurosciences and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Anderson Oliveira SouzaDepartment of Biomolecular Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Evelin Capellari CárnioDepartment of General and Specialized Nursing, College of Nursing of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Adriano SebollelaDepartment of Biochemistry and Immunology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirão Preto, SP, Brazil.
Luciane Carla AlbericiDepartment of Biomolecular Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Maria José Alves RochaDepartment of Basic and Oral Biology, School of Dentistry of Ribeirão Preto, University of São Paulo, Avenida do Café s/n, Ribeirão Preto, SP, CEP 14049-900, Brazil. mjrocha@forp.usp.br.ORCID http://orcid.org/0000-0002-5102-4550
Universidade de São Paulo · BRUniversidade de Ribeirão Preto · BR

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Finance Code 001Fundação de Amparo à Pesquisa do Estado de São Paulo 2015/12152Fundação de Amparo à Pesquisa do Estado de São Paulo 2017/12462-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2018/02854-0
6 · The paper itself

Abstract

Sepsis-associated encephalopathy causes brain dysfunction that can result in cognitive impairments in sepsis survivor patients. In previous work, we showed that simvastatin attenuated oxidative stress in brain structures related to memory in septic rats. However, there is still a need to evaluate the long-term impact of simvastatin administration on brain neurodegenerative processes and cognitive damage in sepsis survivors. Here, we investigated the possible neuroprotective role of simvastatin in neuroinflammation, and neurodegeneration conditions of brain structures related to memory in rats at 10 days after sepsis survival. Male Wistar rats (250-300 g) were submitted to cecal ligation and puncture (CLP, n = 42) or remained as non-manipulated (naïve, n = 30). Both groups were treated (before and after the surgery) by gavage with simvastatin (20 mg/kg) or an equivalent volume of saline and observed for 10 days. Simvastatin-treated rats that survived to sepsis showed a reduction in the levels of nitrate, IL1-β, and IL-6 and an increase in Bcl-2 protein expression in the prefrontal cortex and hippocampus, and synaptophysin only in the hippocampus. Immunofluorescence revealed a reduction of glial activation, neurodegeneration, apoptosis, and amyloid aggregates confirmed by quantification of GFAP, Iba-1, phospho Ser

Indexed as

AnimalsBrainCognitive DysfunctionHydroxymethylglutaryl-CoA Reductase InhibitorsInflammationMaleNeurodegenerative DiseasesRatsRats, WistarSepsisSimvastatinHydroxymethylglutaryl-CoA Reductase InhibitorsSimvastatinAstrocytesEncephalopathyHippocampusMicrogliaNeurodegenerationPrefrontal cortex

Identifiers

PMID32524380
OpenAlexW3032955028

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.