Navegando por Palavras-chave "neuroproteção"
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- ItemAcesso aberto (Open Access)Adenosina e neuroproteção na epilepsia do lobo temporal: da ativação do receptor A1 ao bloqueio do receptor A2A(Liga Brasileira de Epilepsia (LBE), 2010-01-01) Rosim, Fernanda Elisa [UNIFESP]; Silva, Iara Ribeiro [UNIFESP]; Persike, Daniele Suzete [UNIFESP]; Vignoli, Thiago [UNIFESP]; Fernandes, Maria Jose da Silva [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)OBJECTIVE: To characterize the effect of the A2A receptor blockage by the SCH58261 in the seizure modulation and neuroprotection of the brain areas vulnerable to injury by pilocarpine. The effect of SCH58261 was also analyzed in combination with the activation of the A1 receptors by R-Pia. METHODS: Eight groups were studied: Pilo, SCH+Pilo, R-Pia+Pilo, R-Pia+SCH+Pilo, and respective controls. The number of animals in status epilepticus (SE), the latency to the SE onset and the mortality rate were evaluated. The Fluoro Jade B (FJB) method was performed 24 hours and seven days after SE. RESULTS: The pretreatment with SCH58261, R-Pia and R-Pia+SCH58261 reduced the number of animals in SE, increased the latency to the SE and decreased the mortality rate, compared to pilocarpine treatment. The R-Pia and R-Pia+SCH58261 groups exhibited a reduction in the number of FJB stained cells in CA3 and hilus, 24 hours and seven days after SE, and in the piriform cortex only 24 hours after SE, compared to Pilo group. CONCLUSION: The A2A antagonist demonstrated a potent anticonvulsant effect, while the A1 agonist had a crucial role in the seizure modulation and promoted significant neuroprotection.
- ItemSomente MetadadadosAvaliação do efeito neuroprotetor da cafeína em modelo experimental de doença de parkinson: um estudo comportamental, neuroquímico e imunohistoquímico(Universidade Federal de São Paulo (UNIFESP), 2013-12-20) Machado Filho, Joao Ananias [UNIFESP]; Cavalheiro, Esper Abrao Cavalheiro [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease. The occurrence of clinical symptoms is related to the loss of approximately 80% of striatal dopamine and 50% of nigral neurons. Caffeine (CAF) is a methylxanthine with extensive use in medicines and products such as coffee, tea and chocolates, and being assigned neuroprotective activities. This study evaluated neuroprotective effects of caffeine in an animal model of PD induced by 6 - OHDA through behavioral studies, neurochemical and immunohistochemical studies. The animals, male Wistar rats (250-300g) were subjected to three protocols (P1, P2, P3) of striatal lesion by 6-OHDA, with concentration of 24μg/2μL in P1, and 12μg/2μL in P2 and P3. The preventive and curative treatment was done as follows in the these protocols: P1 - CAF treatment (10 and 20mg/kg) for two weeks after the injury (curative); P2 - CAF treatment (10 and 20mg/kg) for two weeks after the injury (curative); another group was treated with CAF (10 mg/kg) and L-Dopa (10mg/kg) after injury (curative); P3 - treated with CAF (5, 10 and 20mg/kg) for two weeks prior to the injury (prophylactic) and continued for two weeks after the injury (curative). The results demonstrate that the 6- OHDA caused an increase in the number of contralateral rotations induced by apomorphine and reduction of striatal dopamine levels with the degree of lesion probably directly related to the dose of 6-OHDA. These effects were reversed by the administration of CAF (10 and 20mg/kg) in P1 and P2, besides being observed increased neuronal viability and immunohystochemical changes that, together, denote neuroprotective activity of CAF in this model. Co-administration of levodopa (10 mg/kg) and CAF (10mg/kg) showed no effect on striatal dopamine concentrations beyond those already observed in the treatment with isolated CAF. CAF (20mg/kg) produced a significant increase in dopamine levels in sham animals and animals lesioned with 6-OHDA. Preventive treatment with caffeine (P3) showed similar results to curative treatment (P2) as observed in the neurochemical and behavioral assessments. Thus, it was demonstrated the neuroprotective effect of caffeine in this experimental study, presenting itself as a potential substance for the prevention and treatment of Parkinson's disease.
- ItemAcesso aberto (Open Access)Epilepsia e neuroproteção: o papel do agonista adenosinérgico A1(RPia) na modulação da crise induzida por pilocarpina(Liga Brasileira de Epilepsia (LBE), 2008-09-01) Silva, Iara Ribeiro [UNIFESP]; Nehlig, Astrid; Rosim, Fernanda Elisa [UNIFESP]; Vignoli, Thiago [UNIFESP]; Persike, Daniele Suzete [UNIFESP]; Blini, João Paulo [UNIFESP]; Cavalheiro, Esper Abrão [UNIFESP]; Sinigaglia-Coimbra, Rita [UNIFESP]; Fernandes, Maria Jose da Silva [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Université Louis Pasteur INSERM Unité 465OBJECTIVE: The aim of this study was to characterize the neuroprotection of the RPia in rats subjected to status epilepticus (SE) induced by pilocarpine (Pilo). METHODS: We evaluated the mismatch between local cerebral glucose utilisation (LCGU) and local cerebral blood flow (LCBF) 4 hours after SE induction. Neuronal loss was evaluated by Fluoro Jade-B (FJB) 24 hours and 90 days after SE. Four groups were studied: Saline, Pilo, RPia+Saline and RPia+Pilo. RESULTS AND CONCLUSIONS: Significant increases in the LCGU were observed in the almost all brain regions of Pilo and RPia+Pilo groups compared to control. However, significant reduction in the LCGU occurred in the substantia nigra pars reticulata and hippocampal formation of RPia+Pilo group versus Pilo. There was significant increase of the LCBF in all the studied areas, comparing the Pilo and RPia+Pilo groups with the control. The increases of LCBF was more intense in rats from RPia+Pilo compared to Pilo, and located mainly in CA2, CA3, dentate gyrus, entorhinal cortex, thalamic nuclei, mammillary body, red nucleus, zone incerta, pontine nucleus and visual cortex. A great number FJB stained cells was observed in the Pilo group and RPia pretreatment reduced the staining in the hippocampal formation, piriform cortex, basolateral amygdala and substantia nigra pars compacta.
- ItemAcesso aberto (Open Access)Selective hypothermia: an experimental study on traumatic brain injury in rats(Academia Brasileira de Neurologia - ABNEURO, 2008-06-01) Dvilevicius, Amylcar Edemilson [UNIFESP]; Prandini, Mirto Nelso [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)OBJECTIVE: To evaluate the efficiency of selective hypothermia in the treatment of the traumatic brain injury in rats. METHOD: After the trauma produced for the model of cortical impact, a small craniectomy in the right frontoparietal region was carried through; after the procedure the animals had been divided in two groups of 15 each. Group A, without treatment with hypothermia (control group) and group B, treated with selective hypothermia for a period to 5 to 6 hours. After this time all the animals were sacrificed, their brains had been removed and histopathological analysis was carried through. RESULTS: Comparison between both groups was done using the counting of neurons injured for field. Counting in the control group n=15 had an average of 70.80 neurons injured for field against an average of 21.33 neurons injured for field in group B (submitted to the treatment with hypothermia), with n=15 also. The difference was statiscally significant. CONCLUSION: Based in the quantification of the neurons injured for field, the effectiveness of the treatment with selective hypothermia was demonstrated.