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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 TNF-α (a and b), IFN-γ (c and d), IL-17 (e and f), IL-1β (g and h), and TGF-β (i and j) levels in the striatum and hippocampus of mice exposed to 6-OHDA. Protein levels of these cytokines were assayed using ELISA kits. Values are expressed as mean ± SEM (n = 6). ∗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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fig4: The effects of two physical training protocols on TNF-α (a and b), IFN-γ (c and d), IL-17 (e and f), IL-1β (g and h), and TGF-β (i and j) levels in the striatum and hippocampus of mice exposed to 6-OHDA. Protein levels of these cytokines were assayed using ELISA kits. Values are expressed as mean ± SEM (n = 6). ∗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: There were high levels of proinflammatory cytokines in the mice that underwent either type of physical training. There was no significant difference in the level of TNF-α in the striatum of TTR and ST mice compared with the Sham group (Figure 4(a)). However, there was a significant increase in the level of TNF-α in the hippocampus of the U + 6-OHDA group compared with the Sham group. When mice were subjected to either type of physical training, a significant decrease in the level of TNF-α was observed (Figure 4(b)). IFN-γ levels in the striatum and hippocampus were increased in the groups exposed to 6-OHDA PD, but the animals that had been subjected to either training model showed a significant decrease in both the hippocampus and striatum (Figures 4(c) and 4(d)). IL-17 levels were increased in the striatum in the U + 6-OHDA group compared with the Sham group (Figure 4(e)) and a decrease in IL-17 levels was observed when the animals were subjected to either type of physical training (Figure 4(e)). No significant difference in the levels of IL-17 was observed in the hippocampus between groups (Figure 4(f)). IL-1β levels in the striatum and hippocampus were increased in the U + 6-OHDA group compared with the Sham group. When 6-OHDA-lesioned mice were subjected to physical training, a significant decrease in IL-1β levels was observed in the hippocampus (Figure 4(h)). There was no significant difference in the level of TGF-β1 in the striatum between groups (Figure 4(i)). There was an increase in TGF-β1 levels in the hippocampus of the U + 6-OHDA group. TGF-β1 levels were significantly reduced when 6-OHDA-lesioned mice were subjected to strength training (Figure 4(j)).


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 TNF-α (a and b), IFN-γ (c and d), IL-17 (e and f), IL-1β (g and h), and TGF-β (i and j) levels in the striatum and hippocampus of mice exposed to 6-OHDA. Protein levels of these cytokines were assayed using ELISA kits. Values are expressed as mean ± SEM (n = 6). ∗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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fig4: The effects of two physical training protocols on TNF-α (a and b), IFN-γ (c and d), IL-17 (e and f), IL-1β (g and h), and TGF-β (i and j) levels in the striatum and hippocampus of mice exposed to 6-OHDA. Protein levels of these cytokines were assayed using ELISA kits. Values are expressed as mean ± SEM (n = 6). ∗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: There were high levels of proinflammatory cytokines in the mice that underwent either type of physical training. There was no significant difference in the level of TNF-α in the striatum of TTR and ST mice compared with the Sham group (Figure 4(a)). However, there was a significant increase in the level of TNF-α in the hippocampus of the U + 6-OHDA group compared with the Sham group. When mice were subjected to either type of physical training, a significant decrease in the level of TNF-α was observed (Figure 4(b)). IFN-γ levels in the striatum and hippocampus were increased in the groups exposed to 6-OHDA PD, but the animals that had been subjected to either training model showed a significant decrease in both the hippocampus and striatum (Figures 4(c) and 4(d)). IL-17 levels were increased in the striatum in the U + 6-OHDA group compared with the Sham group (Figure 4(e)) and a decrease in IL-17 levels was observed when the animals were subjected to either type of physical training (Figure 4(e)). No significant difference in the levels of IL-17 was observed in the hippocampus between groups (Figure 4(f)). IL-1β levels in the striatum and hippocampus were increased in the U + 6-OHDA group compared with the Sham group. When 6-OHDA-lesioned mice were subjected to physical training, a significant decrease in IL-1β levels was observed in the hippocampus (Figure 4(h)). There was no significant difference in the level of TGF-β1 in the striatum between groups (Figure 4(i)). There was an increase in TGF-β1 levels in the hippocampus of the U + 6-OHDA group. TGF-β1 levels were significantly reduced when 6-OHDA-lesioned mice were subjected to strength training (Figure 4(j)).

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