Evidence map›Paper›PMID 21735317›Full record

ArticleNeurotoxicity research2012

Exercise pre-conditioning reduces brain inflammation and protects against toxicity induced by traumatic brain injury: behavioral and neurochemical approach.

Bibiana Castagna Mota, Leticia Pereira, Mauren Assis Souza, Luiz Fernando Almeida Silva, Danieli Valnes Magni, Ana Paula Oliveira Ferreira, Mauro Schneider Oliveira, Ana Flávia Furian, Leidiane Mazzardo-Martins, Morgana Duarte da Silva and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Exploring Molecular Pathways in Exercise-Induced Recovery from Traumatic Brain Injury.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Role of innate inflammation in traumatic brain injury.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Cultivating a healthy neuro-immune network: A health psychology approach.Social and personality psychology compass · 2019
    Article
  20. 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

14 authors at 3 institutions in 1 country.

Bibiana Castagna MotaLaboratório de Bioquímica do Exercício, Departamento de Métodos e Técnicas Desportivas, Centro de Educação Física e Desportos, Universidade Federal de Santa Maria, Santa Maria, RS 97105-900, Brazil.
Leticia Pereira
Mauren Assis Souza
Luiz Fernando Almeida Silva
Danieli Valnes Magni
Ana Paula Oliveira Ferreira
Mauro Schneider Oliveira
Ana Flávia Furian
Leidiane Mazzardo-Martins
Morgana Duarte da Silva
Adair Roberto Soares Santos
Juliano Ferreira
Michele Rechia Fighera
Luiz Fernando Freire Royes
Universidade Federal de Santa Maria · BRUniversidade Federal de Santa Catarina · BRUniversidade Federal do Pampa · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the favorable effects of physical exercise in neurorehabilitation after traumatic brain injury (TBI) are well known, detailed pathologic and functional alterations exerted by previous physical exercise on post-traumatic cerebral inflammation have been limited. In the present study, it is showed that fluid percussion brain injury (FPI) induced motor function impairment, followed by increased plasma fluorescein extravasation and cerebral inflammation characterized by interleukin-1β, tumor necrosis factor-α (TNF-α) increase, and decreased IL-10. In addition, myeloperoxidase (MPO) increase and Na⁺,K⁺-ATPase activity inhibition after FPI suggest that the opening of blood-brain barrier (BBB) followed by neurtrophils infiltration and cerebral inflammation may contribute to the failure of selected targets leading to secondary damage. In fact, Pearson's correlation analysis revealed strong correlation of MPO activity increase with Na⁺,K⁺-ATPase activity inhibition in sedentary rats. Statistical analysis also revealed that previous running exercise (4 weeks) protected against FPI-induced motor function impairment and fluorescein extravasation. Previous physical training also induced IL-10 increase per se and protected against cerebral IL-1β, and TNF-α increase and IL-10 decrease induced by FPI. This protocol of physical training was effective against MPO activity increase and Na⁺,K⁺-ATPase activity inhibition after FPI. The present protection correlated with MPO activity decrease suggests that the alteration of cerebral inflammatory status profile elicited by previous physical training reduces initial damage and limits long-term secondary degeneration after TBI. This prophylactic effect may facilitate functional recovery in patients suffering from brain injury induced by TBI.

Indexed as

AnimalsBehavior, AnimalBlood-Brain BarrierBrain InjuriesCytokinesEncephalitisInterleukin-10Interleukin-1betaMaleMotor ActivityPhysical Conditioning, AnimalRatsRats, WistarSodium-Potassium-Exchanging ATPaseTumor Necrosis Factor-alphaCytokinesInterleukin-10Interleukin-1betaSodium-Potassium-Exchanging ATPaseTumor Necrosis Factor-alpha

Identifiers

PMID21735317
OpenAlexW2034171164

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.