Endurance exercise training protects against the upregulation of nitric oxide in the striatum of MPTP/probenecid mouse model of Parkinson's disease

Al-Jarrah, Muhammed; Obaidat, Heyam; Bataineh, Ziad M.; Walton, Lori Maria; Al-Khateeb, Ahed

doi:10.3233/nre-130831

Cited by 21 publications

(11 citation statements)

References 33 publications

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“…Tuon et al indicated that physical exercise was beneficial in reducing the production of proinflammatory proteins and inflammation in the brain of PD mice [91]. This result is consistent with previous studies by Sung et al and Al-Jarrah et al, which suggested that physical exercise could decrease the level of proinflammatory proteins in the striatum and hippocampus in the PD experimental model through reducing the activity of microglia [147,148].…”

Section: Physical Exercise Can Reduce Inflammation Andsupporting

confidence: 75%

What and How Can Physical Activity Prevention Function on Parkinson’s Disease?

Fan

Jabeen

et al. 2020

Oxidative Medicine and Cellular Longevity

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Aim. This study was aimed at investigating the effects and molecular mechanisms of physical activity intervention on Parkinson’s disease (PD) and providing theoretical guidance for the prevention and treatment of PD. Methods. Four electronic databases up to December 2019 were searched (PubMed, Springer, Elsevier, and Wiley database), 176 articles were selected. Literature data were analyzed by the logic analysis method. Results. (1) Risk factors of PD include dairy products, pesticides, traumatic brain injury, and obesity. Protective factors include alcohol, tobacco, coffee, black tea, and physical activity. (2) Physical activity can reduce the risk and improve symptoms of PD and the beneficial forms of physical activity, including running, dancing, traditional Chinese martial arts, yoga, and weight training. (3) Different forms of physical activity alleviate the symptoms of PD through different mechanisms, including reducing the accumulation of α-syn protein, inflammation, and oxidative stress, while enhancing BDNF activity, nerve regeneration, and mitochondrial function. Conclusion. Physical activity has a positive impact on the prevention and treatment of PD. Illustrating the molecular mechanism of physical activity-induced protective effect on PD is an urgent need for improving the efficacy of PD therapy regimens in the future.

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Section: Physical Exercise Can Reduce Inflammation Andsupporting

confidence: 75%

What and How Can Physical Activity Prevention Function on Parkinson’s Disease?

Fan

Jabeen

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Antiapoptotic effect of exercise in several tissues and experimental models, through its action on the NF-kB pathway, iNOS expression, and NO production, was reported. For instance, exercise attenuates the NF-kB pathway and iNOS activity in the brain, skeletal muscle, blood cells, and gut from humans and rodents (28)(29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

Exercise increases pancreatic β‐cell viability in a model of type 1 diabetes through IL‐6 signaling

et al. 2015

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Type 1 diabetes (T1D) is provoked by an autoimmune assault against pancreatic β cells. Exercise training enhances β-cell mass in T1D. Here, we investigated how exercise signals β cells in T1D condition. For this, we used several approaches. Wild-type and IL-6 knockout (KO) C57BL/6 mice were exercised. Afterward, islets from control and trained mice were exposed to inflammatory cytokines (IL-1β plus IFN-γ). Islets from control mice and β-cell lines (INS-1E and MIN6) were incubated with serum from control or trained mice or medium obtained from 5-aminoimidazole-4 carboxamide1-β-d-ribofuranoside (AICAR)-treated C2C12 skeletal muscle cells. Subsequently, islets and β cells were exposed to IL-1β plus IFN-γ. Proteins were assessed by immunoblotting, apoptosis was determined by DNA-binding dye propidium iodide fluorescence, and NO(•) was estimated by nitrite. Exercise reduced 25, 75, and 50% of the IL-1β plus IFN-γ-induced iNOS, nitrite, and cleaved caspase-3 content, respectively, in pancreatic islets. Serum from trained mice and medium from AICAR-treated C2C12 cells reduced β-cell death, induced by IL-1β plus IFN-γ treatment, in 15 and 38%, respectively. This effect was lost in samples treated with IL-6 inhibitor or with serum from exercised IL-6 KO mice. In conclusion, muscle contraction signals β-cell survival in T1D through IL-6.

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“…Thus, the effects of exercise on inflammatory mediators could be directly associated with the regulation of nitric oxide synthesis and thereby contribute to a reduction in proinflammatory proteins. Previous studies have shown that treadmill training reduces levels of neuronal and inducible nitric oxide synthase in the striatum and hippocampus of experimental models of PD by reducing the activity of microglia [ 57 , 58 ]. Taken together, the results of this study validate the positive effects of physical training on brain pathology in the 6-OHDA mouse model of PD.…”

Section: Discussionmentioning

confidence: 99%

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

Tuon

Souza

Santos

et al. 2015

Oxidative Medicine and Cellular Longevity

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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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Endurance exercise training protects against the upregulation of nitric oxide in the striatum of MPTP/probenecid mouse model of Parkinson's disease

Cited by 21 publications

References 33 publications

What and How Can Physical Activity Prevention Function on Parkinson’s Disease?

What and How Can Physical Activity Prevention Function on Parkinson’s Disease?

Exercise increases pancreatic β‐cell viability in a model of type 1 diabetes through IL‐6 signaling

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

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