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Katiane Santin,
Ricardo Fagundes da Rocha,
Fernanda Cechetti,
André Quincozes-Santos,
Daniela Fraga de Souza,
Patrícia Nardin,
Letícia Rodrigues,
Marina Concli Leite,
José Cláudio Fonseca Moreira,
Christianne Gazzana Salbego,
Carlos Alberto Gonçalves
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ABSTRACT: Physical activity has been related to antioxidant adaptations, which is associated with health benefits, including those to the nervous system. Additionally, available data suggest exercise and a caloric restriction regimen may reduce both the incidence and severity of neurological disorders. Therefore, our aim was to compare hippocampal redox status and glial parameters among sedentary, trained, caloric-restricted sedentary and caloric-restricted trained rats. Forty male adult rats were divided into 4 groups: ad libitum-fed sedentary (AS), ad libitum-fed exercise training (AE), calorie-restricted sedentary (RS) and calorie-restricted exercise training (RE). The caloric restriction (decrease of 30% in food intake) and exercise training (moderate in a treadmill) were carried out for 3 months. Thereafter hippocampus was surgically removed, and then redox and glial parameters were assessed. Increases in reduced glutathione (GSH) levels and total antioxidant reactivity (TAR) were observed in AE, RS and RE. The nitrite/nitrate levels decreased only in RE. We found a decrease in carbonyl content in AE, RS and RE, while no modifications were detected in thiobarbituric acid reactive substances (TBARS). Total reactive antioxidant potential (TRAP), superoxide dismutase (SOD) activity, S100B and glial fibrilary acid protein (GFAP) content did not change, but caloric restriction was able to increase glutamine synthetase (GS) activity in RS and glutamate uptake in RS and RE. Exercise training, caloric restriction and both combined can decrease oxidative damage in the hippocampus, possibly involving modulation of astroglial function, and could be used as a strategy for the prevention of neurodegenerative diseases.
Brain research 11/2011; 1421:1-10. · 2.46 Impact Factor
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ABSTRACT: Boldine is one of the most potent natural antioxidants and displays some important pharmacological activities, such as cytoprotective and anti-inflammatory activities, which may arise from its free radical scavenging properties. Given that the pathogenesis of brain ischemia/reperfusion has been associated with an excessive generation of oxygen free radicals, the aim of this study was to evaluate the neuroproperties of boldine using hippocampal slices from Wistar rats exposed to oxygen and glucose deprivation (OGD), followed by reoxygenation, to mimic an ischemic condition. The OGD ischemic condition significantly impaired cellular viability, increased lactate dehydrogenase (LDH) leakage and increased free radical generation. In non-OGD slices, incubation with 100microM boldine significantly increased LDH released into incubation media and decreased mitochondrial activity, suggesting an increase of tissue damage caused by boldine. However, slices incubated with 10microM boldine during and after OGD exposure had significantly increased cellular viability with no effect on cell damage. Total reactive antioxidant potential (TRAP) levels measured for this alkaloid showed an antioxidant potential three times higher than Trolox, which acts as a peroxyl radical scavenger. Moreover, boldine prevented the increase in lipoperoxidation levels induced by ischemia, but higher concentrations potentiated this parameter. These results confirm the potent antioxidant properties of this alkaloid, and add evidence to support the need for further investigations in order to confirm the potential pro-oxidant effects of boldine at higher doses.
NeuroToxicology 07/2008; 29(6):1136-40. · 3.10 Impact Factor
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ABSTRACT: We have recently demonstrated that high intensity training exercise exacerbates brain damage, while a moderate intensity (2 weeks of 20 min/day of treadmill training) reduces the injury caused by in vitro ischemia, oxygen and glucose deprivation (OGD), to hippocampal slices from Wistar rats. In the present paper, the effect of different running programs on severity of ischemic OGD lesion was examined, by the evaluation of three protocols designed to simulate exercise conditions common to humans: one or three 20-min sessions per week, during 12 weeks (moderate intensity), and two 20-min daily sessions for 3 weeks. OGD caused an increase of lactate dehydrogenase (LDH) release into the incubation media, a marker of tissue necrosis, and a decline of cell viability, as assessed by the decrease of mitochondrial dehydrogenase activity (MTT method). Moderate exercise, three times a week during 12-week treadmill training, decreased LDH release after OGD, while one weekly session and 3 weeks of two daily sessions did not affect OGD-induced LDH released. No exercise protocol evaluated altered MTT reduction. Our data support the hypothesis that moderate intensity exercise reduces hippocampal susceptibility to in vitro ischemia.
Brain Research 08/2007; 1157:121-5. · 2.73 Impact Factor
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ABSTRACT: In the present study we investigated the toxicity induced by exposing organotypic slice culture to beta-amyloid peptide 25-35 (25microM) for 1, 3, 6, 12, 24 and 48h. To elucidate a mechanism involved in its toxicity, we studied the PI3-K cell signaling pathway, particularly Akt/PKB, GSK-3beta, and PTEN proteins. Cell death was quantified by propidium iodide uptake and proteins were analyzed by immunoblotting. Our results showed a significant cell death after 48h of beta-amyloid 25-35 peptide exposition. The exposition of cultures to beta-amyloid peptide resulted in an increase in the phosphorylation state of Akt and GSK-3beta proteins after 6h, followed by a decrease of the phosphorylation state of these proteins after 12h of exposition. However, after 24h of peptide treatment, the phosphorylation of GSK-3beta presented a new increase while the phosphorylation of Akt remained down. The immunocontent of the PTEN protein, an indirect Akt phosphatase, increased after 24 and 48h of beta-amyloid exposition. These results suggest an involvement of Akt dephosphorylation/inactivation in the toxicity induced by the beta-amyloid 25-35 peptide in organotypic slice hippocampal culture, probably induced by increasing PTEN immunocontent. Taken together, our results provide more information about the molecular mechanisms involved on beta-amyloid peptide toxicity.
Neurochemistry International 02/2007; 50(1):229-35. · 2.86 Impact Factor
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ABSTRACT: In the present study we investigated the toxicity induced by exposing organotypic slice culture to β-amyloid peptide 25–35 (25 μM) for 1, 3, 6, 12, 24 and 48 h. To elucidate a mechanism involved in its toxicity, we studied the PI3-K cell signaling pathway, particularly Akt/PKB, GSK-3β, and PTEN proteins. Cell death was quantified by propidium iodide uptake and proteins were analyzed by immunoblotting. Our results showed a significant cell death after 48 h of β-amyloid 25–35 peptide exposition. The exposition of cultures to β-amyloid peptide resulted in an increase in the phosphorylation state of Akt and GSK-3β proteins after 6 h, followed by a decrease of the phosphorylation state of these proteins after 12 h of exposition. However, after 24 h of peptide treatment, the phosphorylation of GSK-3β presented a new increase while the phosphorylation of Akt remained down. The immunocontent of the PTEN protein, an indirect Akt phosphatase, increased after 24 and 48 h of β-amyloid exposition. These results suggest an involvement of Akt dephosphorylation/inactivation in the toxicity induced by the β-amyloid 25–35 peptide in organotypic slice hippocampal culture, probably induced by increasing PTEN immunocontent. Taken together, our results provide more information about the molecular mechanisms involved on β-amyloid peptide toxicity.
Neurochemistry International.
