Navegando por Palavras-chave "doença de parkinson"

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    Avaliação 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.