Physical Training Regulates Mitochondrial Parameters and Neuroinflammatory Mechanisms in an Experimental Model of Parkinson's Disease. (10th September 2015)
- Record Type:
- Journal Article
- Title:
- Physical Training Regulates Mitochondrial Parameters and Neuroinflammatory Mechanisms in an Experimental Model of Parkinson's Disease. (10th September 2015)
- Main Title:
- Physical Training Regulates Mitochondrial Parameters and Neuroinflammatory Mechanisms in an Experimental Model of Parkinson's Disease
- Authors:
- Tuon, Talita
Souza, Priscila S.
Santos, Marcela F.
Pereira, Fernanda T.
Pedroso, Giulia S.
Luciano, Thais F.
De Souza, Claudio T.
Dutra, Rafael C.
Silveira, Paulo C. L.
Pinho, Ricardo A. - Other Names:
- Yan Liang-Jun Academic Editor.
- Abstract:
- 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- κ B) p65, and sirtuin 1 (Sirt1) by western blot; tumor necrosis factor- α (TNF- α ), interleukin-1 β (IL-1 β ), IL-17, interferon- γ (IFN- γ ), and transforming growth factor β 1 (TGF- β 1) levels by ELISA; NO content; and complex I (CI) activity. STR + 6-OHDA mice had higher TH levels and CI activity and lower NF- κ B 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- κ B p65, TNF- α, IFN- γ, IL-1 β, and TGF- β 1Abstract : 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- κ B) p65, and sirtuin 1 (Sirt1) by western blot; tumor necrosis factor- α (TNF- α ), interleukin-1 β (IL-1 β ), IL-17, interferon- γ (IFN- γ ), and transforming growth factor β 1 (TGF- β 1) levels by ELISA; NO content; and complex I (CI) activity. STR + 6-OHDA mice had higher TH levels and CI activity and lower NF- κ B 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- κ B p65, TNF- α, IFN- γ, IL-1 β, and TGF- β 1 levels in 6-OHDA mice, while treadmill exercise increased CI activity and NO, TH, and Sirt1 levels and reduced NF- κ B p65, TNF- α, IFN- γ, and IL-1 β 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- κ B p65. Changes in nitric oxide levels may also be a mechanism by which 6-OHDA-induced inflammation is controlled. … (more)
- Is Part Of:
- Oxidative medicine and cellular longevity. Volume 2015(2015)
- Journal:
- Oxidative medicine and cellular longevity
- Issue:
- Volume 2015(2015)
- Issue Display:
- Volume 2015, Issue 2015 (2015)
- Year:
- 2015
- Volume:
- 2015
- Issue:
- 2015
- Issue Sort Value:
- 2015-2015-2015-0000
- Page Start:
- Page End:
- Publication Date:
- 2015-09-10
- Subjects:
- Oxidative stress -- Periodicals
Cells -- Aging -- Periodicals
Cells -- Aging
Oxidative stress
Oxidative Stress -- Periodicals
Cell Aging -- Periodicals
Periodicals
611.0181 - Journal URLs:
- https://www.hindawi.com/journals/omcl/ ↗
- DOI:
- 10.1155/2015/261809 ↗
- Languages:
- English
- ISSNs:
- 1942-0900
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 10310.xml