Cited by 92Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

Physical Training Regulates Mitochondrial Parameters and Neuroinflammatory Mechanisms in an Experimental Model of Parkinson’s Disease

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Tuon, Talita, Souza, Priscila S., Santos, Marcela F., Pereira, Fernanda T., Pedroso, Giulia S., Luciano, Thais F., De Souza, Claudio T., Dutra, Rafael C. +2 more·2015·Oxidative Medicine and Cellular Longevity

Abstract

This study aimed to evaluate the effects of two different protocols for physical exercise (strength and aerobic training) on mitochondrial and inflammatory parameters in the 6-OHDA experimental model of Parkinson's disease. Six experimental groups were used (n = 12 per group): untrained + vehicle (Sham), strength training + vehicle (STR), treadmill training + vehicle (TTR), untrained + 6-OHDA (U + 6-OHDA), strength training + 6-OHDA (STR + 6-OHDA), and treadmill training + 6-OHDA (TTR + 6-OHDA). The mice were subjected to strength or treadmill training for 8 weeks. PD was induced via striatal injection of 6-OHDA 24 h after the last exercise session. Mice were euthanized by cervical dislocation and the striatum and hippocampus were homogenized to determine levels of tyrosine hydroxylase (TH), nuclear factor kappa B (NF-κB) p65, and sirtuin 1 (Sirt1) by western blot; tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-17, interferon-γ (IFN-γ), and transforming growth factor β1 (TGF-β1) levels by ELISA; NO content; and complex I (CI) activity. STR + 6-OHDA mice had higher TH levels and CI activity and lower NF-κB p65 and IFN-γ levels in the striatum compared to U + 6-OHDA mice, while TTR + 6-OHDA mice had higher Sirt1 levels and CI activity in both the striatum and the hippocampus, compared to U + 6-OHDA mice. Strength training increased CI activity and TH and Sirt1 levels and reduced NO, NF-κB p65, TNF-α, IFN-γ, IL-1β, and TGF-β1 levels in 6-OHDA mice, while treadmill exercise increased CI activity and NO, TH, and Sirt1 levels and reduced NF-κB p65, TNF-α, IFN-γ, and IL-1β levels. Our results demonstrated that both treadmill training and strength training promote neuroprotection, possibly by stimulating Sirt1 activity, which may in turn regulate both mitochondrial function and neuroinflammation via deacetylation of NF-κB p65. Changes in nitric oxide levels may also be a mechanism by which 6-OHDA-induced inflammation is controlled.

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Authors
Tuon, T., Souza, P. S., Santos, M. F., Pereira, F. T., Pedroso, G. S., Luciano, T. F., De Souza, C. T., Dutra, R. C., Silveira, P. C. L., & Pinho, R. A.
Affiliations
  • Universidade do Extremo Sul Catarinense (BR)
  • Laboratory of Exercise Biochemistry and Physiology, Graduate Program in Health Sciences, Health Sciences Unit, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil
  • Universidade Federal de Santa Catarina (BR)
Corresponding author
Pinho, Ricardo A.
Venue
Oxidative Medicine and Cellular Longevity
Publisher
Wiley
Published
2015
Volume
2015
Pages
1-10
ISSN
  • 1942-0994 (ISSN-L)
  • 1942-0900
OpenAlex
W1799639810
Cited by
92
References
5
Citations by year
2026: 7 · 2025: 7 · 2024: 11 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 19 · 2019: 10 · 2018: 4 · 2017: 6 · 2016: 6
FWCI
3.76
Type
journal article
Language
en
Open access
Locations
  • Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Universidade do Extremo Sul Catarinense
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico
  • Fundação de Apoio à Pesquisa Científica e Tecnológica do Estado de Santa Catarina
  • NENASC
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords
Parkinson's disease, physical activity, resistance training, treadmill training, aerobic exercise, mitochondrial function, complex I activity, neuroinflammation, 6-hydroxydopamine, neuroprotection, SIRT1, NF-κB p65, tyrosine hydroxylase, nitric oxide, striatum, hippocampus, cytokines, neurodegeneration model, mice
MeSH terms
Animals, Male, Mice, Inbred C57BL, Mitochondria, Models, Theoretical, Motor Activity, Parkinson Disease, Mice

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