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

Tuon T, Souza PS, Santos MF, Pereira FT, Pedroso GS, Luciano TF, De Souza CT, Dutra RC, Silveira PC, Pinho RA - Oxid Med Cell Longev (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Exercise Biochemistry and Physiology, Graduate Program in Health Sciences, Health Sciences Unit, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil.

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.

No MeSH data available.


Related in: MedlinePlus

The effects of two physical training protocols on nitric oxide (a and b, n = 6) and NF-κB p65 (c and d, n = 3) levels in the striatum and hippocampus of mice exposed to 6-OHDA. For western blotting, hippocampus and striatum protein extracts containing 0.2 mg total protein were separated by SDS-PAGE, transferred to nitrocellulose membranes, and probed with anti-NF-κB-p65 antibody. Nitrite generation by NO was assayed spectrophotometrically. Values for NF-κB p65 are presented as mean area × intensity of bands ± SEM (arbitrary units), and oxide nitric levels are expressed as mean ± SEM. ∗P < 0.05, Sham versus U + 6-OHDA; #P < 0.05, U + 6-OHDA versus training groups plus 6-OHDA. 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).
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fig3: The effects of two physical training protocols on nitric oxide (a and b, n = 6) and NF-κB p65 (c and d, n = 3) levels in the striatum and hippocampus of mice exposed to 6-OHDA. For western blotting, hippocampus and striatum protein extracts containing 0.2 mg total protein were separated by SDS-PAGE, transferred to nitrocellulose membranes, and probed with anti-NF-κB-p65 antibody. Nitrite generation by NO was assayed spectrophotometrically. Values for NF-κB p65 are presented as mean area × intensity of bands ± SEM (arbitrary units), and oxide nitric levels are expressed as mean ± SEM. ∗P < 0.05, Sham versus U + 6-OHDA; #P < 0.05, U + 6-OHDA versus training groups plus 6-OHDA. 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).

Mentions: Striatal and hippocampal NO were increased in the U + 6-OHDA group compared with the Sham group. When mice were subjected to treadmill physical training (TTR + 6-OHDA), NO levels were significantly decreased compared with the U + 6-OHDA group (Figures 3(a) and 3(b)) in the hippocampus and striatum. The levels of total NF-κB p65 protein in the striatum and hippocampus increased in the U + 6-OHDA group. In the striatum, a significant decrease was observed in both the STR + 6-OHDA and TTR + 6-OHDA trained groups (Figure 3(c)), while, in the hippocampus, a significant decrease in the levels of total NF-κB p65 protein was detected only in the STR + 6-OHDA group compared with the U + 6-OHDA group (Figure 3(d)).


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

Tuon T, Souza PS, Santos MF, Pereira FT, Pedroso GS, Luciano TF, De Souza CT, Dutra RC, Silveira PC, Pinho RA - Oxid Med Cell Longev (2015)

The effects of two physical training protocols on nitric oxide (a and b, n = 6) and NF-κB p65 (c and d, n = 3) levels in the striatum and hippocampus of mice exposed to 6-OHDA. For western blotting, hippocampus and striatum protein extracts containing 0.2 mg total protein were separated by SDS-PAGE, transferred to nitrocellulose membranes, and probed with anti-NF-κB-p65 antibody. Nitrite generation by NO was assayed spectrophotometrically. Values for NF-κB p65 are presented as mean area × intensity of bands ± SEM (arbitrary units), and oxide nitric levels are expressed as mean ± SEM. ∗P < 0.05, Sham versus U + 6-OHDA; #P < 0.05, U + 6-OHDA versus training groups plus 6-OHDA. 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).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4581546&req=5

fig3: The effects of two physical training protocols on nitric oxide (a and b, n = 6) and NF-κB p65 (c and d, n = 3) levels in the striatum and hippocampus of mice exposed to 6-OHDA. For western blotting, hippocampus and striatum protein extracts containing 0.2 mg total protein were separated by SDS-PAGE, transferred to nitrocellulose membranes, and probed with anti-NF-κB-p65 antibody. Nitrite generation by NO was assayed spectrophotometrically. Values for NF-κB p65 are presented as mean area × intensity of bands ± SEM (arbitrary units), and oxide nitric levels are expressed as mean ± SEM. ∗P < 0.05, Sham versus U + 6-OHDA; #P < 0.05, U + 6-OHDA versus training groups plus 6-OHDA. 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).
Mentions: Striatal and hippocampal NO were increased in the U + 6-OHDA group compared with the Sham group. When mice were subjected to treadmill physical training (TTR + 6-OHDA), NO levels were significantly decreased compared with the U + 6-OHDA group (Figures 3(a) and 3(b)) in the hippocampus and striatum. The levels of total NF-κB p65 protein in the striatum and hippocampus increased in the U + 6-OHDA group. In the striatum, a significant decrease was observed in both the STR + 6-OHDA and TTR + 6-OHDA trained groups (Figure 3(c)), while, in the hippocampus, a significant decrease in the levels of total NF-κB p65 protein was detected only in the STR + 6-OHDA group compared with the U + 6-OHDA group (Figure 3(d)).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Exercise Biochemistry and Physiology, Graduate Program in Health Sciences, Health Sciences Unit, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil.

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.

No MeSH data available.


Related in: MedlinePlus