Efeito Neuroprotetor da N - acetilcisteína sobre a neuropatia alcoólica induzida experimentalmente em ratos

• Ano de defesa: 2015
• Autor(a) principal: Hösch, Natália Gabriele
• Orientador(a): Ventura, Jalile Amin Naves
• Banca de defesa: Souza, Guilherme Rabelo De, Brigagão, Maísa Ribeiro Pereira Lima
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Alfenas
• Programa de Pós-Graduação: Programa Multicêntrico de Pós-Graduação em Ciências Fisiológicas
• Departamento: Instituto de Ciências Biomédicas
• País: Brasil
• Palavras-chave em Português: Neuropatia alcoólica; Etanol; Acetilcosteína
• Área do conhecimento CNPq: FISIOLOGIA DE ORGAOS E SISTEMAS::NEUROFISIOLOGIA
• Link de acesso: https://repositorio.unifal-mg.edu.br/handle/123456789/580

Chronic alcohol consumption produces a painful peripheral neuropathy which is characterized by spontaneous burning pain, hyperalgesia and allodynia. Scientific evidences support oxidative stress as the biochemical trigger for the development of alcoholic neuropathy, since alcohol consumption increases the amounts of free radicals and damage biochemical structures, in addition to deplete endogenous antioxidant reserves. N - acetylcysteine (NAC) is an antioxidant agent that facilitates the biosynthesis of glutathione and capture reactive oxygen species. Therefore, the aim of this study was to investigate the protective effect of NAC on induced alcoholic neuropathy. Wistar rats were divided into 4 experimental groups (Control group, Ethanol group, NAC + Ethanol group and NAC group) containing an average of 10 animals each group. Nociceptive tests, Randall Selitto (mechanical hyperalgesia), Tail flick (thermal hyperalgesia) and electronic von Frey (allodynia) were performed at the day called 0 (before treatment) and at the fourth, sixth, eighth and tenth weeks. Rota-rod test was also performed to assess the balance and motor coordination of the animals, at day zero and at the tenth week. Immunofluorescence investigated the expression of c - Fos at brain areas associated with nociception (Paraventricular Nucleus of Hypothalamus (PVN), Dorsal Raphe Nuclei (DRN) and Periaqueductal Gray (PAG)). Results showed that Ethanol group showed a significant decrease in the nociceptive threshold, as evidenced from the reduced latency time in Tail flick test and decreased paw withdrawal threshold in Randall Sellito test and electronic von Frey compared to the mean baseline (day 0). NAC + Ethanol group at 10th week, in turn, maintained a high thermal nociceptive threshold at Tail flick test and also retained high mechanical nociceptive threshold at Randall Selitto and electronic von Frey relative to Ethanol group. A decrease in the falling latency at Rota-rod test was observed in the ethanol group after 10 weeks of treatment compared to day 0. However, NAC + Ethanol group kept the high values of falling latency compared to Ethanol group. Immunofluorescence tests showed, for Ethanol group, a significant increase in the number of immunoreactive neurons for c-Fos in DRN, PVN and PAG if compared to Control group. Once again, NAC prevented the increase induced by ethanol. Thus, these results suggest that NAC exerts a neuroprotective and an antinociceptive effect in alcoholic neuropathy.