Exercício físico como fator neuroprotetor em um modelo progressivo de parkinsonismo induzido por reserpina em ratos

• Ano de defesa: 2023
• Autor(a) principal: Silva, Marcelo Nunes da
• Orientador(a): Santos, José Ronaldo dos
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Programa de Pós-Graduação: Pós-Graduação em Ciências Fisiológicas
• Palavras-chave em Português: Doença de Parkinson; Atividade física; Neuroproteção; Dopamina; Parkinson's disease; Physical activity; Neuroprotection; Dopamine
• Área do conhecimento CNPq: CIENCIAS BIOLOGICAS::FISIOLOGIA
• Link de acesso: http://ri.ufs.br/jspui/handle/riufs/17526

Introduction: Parkinson's disease (PD) is a chronic and progressive neurodegenerative disease mainly related to the death of dopaminergic neurons. The treatment is carried out with drugs that promote the more significant activity of the dopaminergic pathway; however, PD has no cure. Non-pharmacological strategies have been studied to delay the onset of the disease, minimize symptoms, or both. Among these strategies, physical exercise stands out for promoting neuroprotection. Thus, the present study evaluated whether physical exercise acts as a neuroprotective factor in a progressive model of parkinsonism induced by reserpine (RES) in rats. Method: 48 male Wistar rats, aged 6-7 months old, weighing 350-450 g, were used with authorization from the Ethics Committee for Research with Animals of the Federal University of Sergipe (protocol number: 5483070122). Animals were allocated into six groups (n = 8 per group): 1) CTR-Sedentary (CTR-SED), 2) RES-Sedentary (RESSED), 3) CTR-Exercise (CTR-EXE), 4) RES-Exercise Prior (RES-EXE-PRE), 5) RESSynchronous Exercise (RES-EXE-SIN) and 6) RES-Delayed Exercise (RES-EXETAR). Animals received ten subcutaneous injections of vehicle (CTR groups) or RES 0.1 mg/kg (RES groups), one every 48h. Animals in groups 1 and 2 were not submitted to physical exercise sessions. Animals in groups 3 and 4 were submitted to physical exercise sessions 15 days before starting the vehicle or RES injections. The animals in group 5 started the physical exercise sessions concomitantly with the beginning of the injections with RES. The animals in group 6 only started the physical exercise sessions 48h after the sixth RES injection. Throughout the treatment, the animals were submitted to behavioral tests: (a) catalepsy test (every 48h), (b) oral movements (days 14 and 20), and open field test (days 8 and 20). Throughout the experiment, the body mass of the animals was also measured. On day 20, the rats were anesthetized and perfused; their brains were removed and subjected to immunohistochemistry for Tyrosine Hydroxylase (TH). Results: Prior physical exercise was able to delay the onset of motor changes induced by RES in the catalepsy test. Besides, the animals in all groups with exercise showed a lower disease progression. Prior exercise was also able to prevent anxiety-like behavior (open field - day 8); and partially prevent motor damage in the oral movement, in the open field test, and loss of body mass. Only animals with prior exercise did not present a reduction in immunoreactivity for tyrosine hydroxylase (TH), an enzyme involved in the dopamine synthesis pathway. Conclusion: our study suggests that physical exercise promotes a neuroprotective effect, slowing the progression of parkinsonism induced by RES in rats.