Evidence map›Paper›PMID 27796742›Full record

ArticleMolecular neurobiology2017

Brain Oxidative Stress During Experimental Sepsis Is Attenuated by Simvastatin Administration.

Carlos Henrique Rocha Catalão, Nilton Nascimento Santos-Júnior, Luís Henrique Angenendt da Costa, Anderson Oliveira Souza, Luciane Carla Alberici, Maria José Alves Rocha

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

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  11. 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

6 authors at 1 institution in 1 country.

Carlos Henrique Rocha CatalãoDepartment of Neurosciences and Behavioral Sciences of Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Nilton Nascimento Santos-JúniorDepartment of Neurosciences and Behavioral Sciences of Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Luís Henrique Angenendt da CostaDepartment of Neurosciences and Behavioral Sciences of Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Anderson Oliveira SouzaDepartment of Physics and Chemistry, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Luciane Carla AlbericiDepartment of Physics and Chemistry, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Maria José Alves RochaDepartment of Morphology, Physiology and Basic Pathology, School of Dentistry of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil. mjrocha@forp.usp.br.
Universidade de São Paulo · BR

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo 2010/17259-9Fundação de Amparo à Pesquisa do Estado de São Paulo 2015/12152
6 · The paper itself

Abstract

During sepsis, brain damage is associated with oxidative stress due to overproduction of reactive oxygen species (ROS). Although there are recent reports about the benefits of statins in experimental sepsis and endotoxemia in peripheral organs, little is known about their effects in the CNS. Here, we investigated the antioxidant properties of simvastatin and its possible neuroprotective role during experimental sepsis. Male Wistar rats (250-300 g) were submitted to cecal ligation and puncture (CLP, n = 34) or remained as non-manipulated (naive, n = 34). Both groups were treated by gavage with simvastatin (20 mg/kg) or an equivalent volume of saline. The animals submitted to CLP were treated 4 days before and 48 h after surgery. One animal group was decapitated and the blood and brain were collected to quantify plasma levels of cytokines and assess astrogliosis and apoptosis in the prefrontal cortex and hippocampus. Another group was perfused with PBS (0.01 M), and the same brain structures were dissected to analyze oxidative damage. The CLP rats treated with simvastatin showed a reduction in nitric oxide (P < 0.05), IL1-β (P < 0.001), IL-6 (P < 0.01), and TBARS levels (P < 0.001) and an increase in catalase activity (P < 0.01), citrate synthase enzyme (P < 0.05), and normalized GSH/GSSG ratio. In addition, the histopathological analysis showed a reduction (P < 0.001) in reactive astrocytes and caspase 3-positive apoptotic cells. The results suggest a possible neuroprotective effect of simvastatin in structures responsible for spatial learning and memory and indicate the need for behavioral studies evaluating the impact on cognitive damage, as frequently seen in patients surviving sepsis.

Indexed as

AnimalsApoptosisBrainCaspase 3CecumCitrate (si)-SynthaseCytokinesGlial Fibrillary Acidic ProteinHippocampusLigationMaleModels, BiologicalNitratesOxidative StressPrefrontal CortexPuncturesCaspase 3Citrate (si)-SynthaseCytokinesGlial Fibrillary Acidic ProteinNitratesSimvastatinThiobarbituric Acid Reactive SubstancesAntioxidantsHMG-CoA inhibitorsROSSeptic encephalopathy

Identifiers

PMID27796742
OpenAlexW2546000389

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.