Avaliação morfológica e molecular dos músculos masseter e temporal de ratos Wistar submetidos à privação do sono paradoxal

Detalhes bibliográficos
Ano de defesa: 2019
Autor(a) principal: Yujra, Veronica Quispe [UNIFESP]
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Tese
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=8474540
https://repositorio.unifesp.br/handle/11600/59528
Resumo: This study will be presented in four Chapters. The first reviews the role of healthy sleep in cellular and tissue homeostasis, as well as clinical and experimental studies that showed possible mechanisms responsible for muscle atrophy as result from sleep deprivation. This process is few studied in Dentistry, an area in which sleep deprivation has not clarified the role of inflammation and/or degeneration of the masticatory muscles, in addition to having a direct relationship with dysfunctions in the stomatognathic system. Objective: Evaluate the influence of paradoxical sleep deprivation and rebound sleep on masseter and temporal muscles of Wistar rats. Methodology: Three experimental groups were used: Control = CTL, 96-hour sleep deprived group (SD) and Rebound (SD + R) group submitted to SD + 96-hour rebound sleep protocol. After euthanasia, masseter and temporal muscles were analyzed in the following aspects: morphological (HE, cross-sectional area, myofiber density); inflammatory (Western Blotting for Toll Like pathway, real-time PCR for TNF, COX-2, iNOS and immunohistochemistry for TNF); atrophic by the expression of MuRF and MAFbx; by MyOD and, myogenin immunoexpression and finally by synthesis pathway activation of the Akt / p70S6 and autophagic degradation for LC3 / P62 by the Western Blotting assay. Results: These are described in Chapters II and III. In Article A, we show that under the sleep deprivation masseter muscle expressed less histomorphometric changes and inhibited the Toll-like inflammatory pathway. The temporal muscle had higher signs of inflammation and also showed overexpression of the MAFbx atrophic gene (p <0.05). In article B, we noted that in SD groups, both muscles showed TNF hyperexpression (p<0.05), with modulation in SD + R, the same occurred in the myogenic activity of MyoD and Myogenin. Finally the analysis of protein turn-over indicated that Akt protein was decreased only in temporal (p <0.05) while LC3 degradation protein increased for both muscles after SD. Conclusion: In Chapter IV, grouped the general conclusions, the sleep deprivation induced changes in the masseter and temporal muscles of rats. The findings showed greater responsiveness of the temporal muscle in the activation of inflammatory and atrophic pathways, as well as inhibition of the main routes of synthesis, this evidenced of less adaptive capacity than the masseter and suggested greater relevance in the study of the effects of experimental sleep deprivation.