Atividade inflamatória e apoptótica em glândulas salivares de ratos induzidas pela privação de sono paradoxal
Arquivos
Data
2021-12-01
Autores
Souza, Ana Carolina Flygare 
Orientadores
Ribeiro, Daniel Araki
Tipo
Tese de doutorado
Título da Revista
ISSN da Revista
Título de Volume
Resumo
O objetivo do presente trabalho foi avaliar se a privação de sono paradoxal é capaz de deflagrar processo inflamatório e apoptose nas glândulas parótida e submandibular de ratos Wistar. Foram utilizados 24 ratos Wistar machos sendo distribuídos nos seguintes grupos: Grupo 1-Controle (CTRL; n=8): os animais não foram submetidos a quaisquer procedimentos; Grupo 2-Privação do Sono (PS; n=8): os animais foram submetidos a Privação de Sono Paradoxal por 96h e Grupo 3-Rebote (R; n=8): os animais foram privados de sono 96 horas, seguido por um período de 96 horas sem intervenção. Foram avaliados os seguintes parâmetros: análise histopatológica, as proteínas: Ki-67, COX-2 e Caspase-3 através de imuno-histoquímica, expressão de TNF-α, Interleucina 6 (IL-6), interleucina 10 (IL-10) e Citocromo C por PCR em tempo real. Os resultados revelaram atrofia acinar, presença de vacúolos e células em apoptose na glândula parótida e presença de vacúolos e desorganização dos ácinos mucosos na glândula submandibular no grupo PS. A expressão das interleucinas 6, 10 e do TNF-ɑ foi diferencialmente expressa nos grupos PS e R tanto na parótida como na submandibular. A apoptose foi acionada nas duas glândulas, sendo que na submandibular aconteceu de forma mais intensa, pois se detectou aumento não somente da expressão da caspase-3 ativada como também do citocromo C. A proliferação celular foi também detectada por meio da marcação de Ki-67 nos grupos R das duas glândulas. Em suma, a privação de sono é capaz de deflagrar processo inflamatório, bem como ativar a apoptose nas glândulas salivares maiores de ratos.
The purpose of the present work was to evaluate if paradoxical sleep deprivation is able to trigger inflammatory process and apoptosis in the parotid and submandibular glands of Wistar rats. Twenty-four male Wistar rats were distributed in the following groups: Group 1-Control (CTRL; n=8): the animals were not submitted to any procedures; Group 2-Sleep deprivation (PS; n=8): the animals were submitted to Paradoxal Sleep deprivation for 96h and Group 3-Rebote (R; n=8): the animals were sleep deprived for 96 hours, followed by a period of 96 hours without any intervention. The following parameters were evaluated: histopathological analysis, immunohistochemistry for Ki-67, COX-2 and Caspase-3 antibodies and expression of TNF-α, Interleukin 6 (IL-6), Interleukin 10 (IL-10) and Citochrome C by real-time PCR. The results revealed acinar atrophy, presence of vacuoles and apoptotic cells in the parotid gland and presence of vacuoles and disorganization of mucous acinus in the submandibular gland in the PS group. The expression of interleukins 6, 10 and TNF-ɑ was differentially expressed in the PS and R groups both in the parotid and submandibular glands. Apoptosis was triggered in both salivary glands, being in the submandibular gland in a more intense way, because it was detected an increase not only in the activated caspase-3 expression but also in the cytochrome C. The cellular proliferation was also detected by means of Ki-67 immunoexpression in the R groups of the two salivary glands. In short, sleep deprivation is able to trigger an inflammatory process, as well as activate apoptosis in the major salivary glands of rats.
The purpose of the present work was to evaluate if paradoxical sleep deprivation is able to trigger inflammatory process and apoptosis in the parotid and submandibular glands of Wistar rats. Twenty-four male Wistar rats were distributed in the following groups: Group 1-Control (CTRL; n=8): the animals were not submitted to any procedures; Group 2-Sleep deprivation (PS; n=8): the animals were submitted to Paradoxal Sleep deprivation for 96h and Group 3-Rebote (R; n=8): the animals were sleep deprived for 96 hours, followed by a period of 96 hours without any intervention. The following parameters were evaluated: histopathological analysis, immunohistochemistry for Ki-67, COX-2 and Caspase-3 antibodies and expression of TNF-α, Interleukin 6 (IL-6), Interleukin 10 (IL-10) and Citochrome C by real-time PCR. The results revealed acinar atrophy, presence of vacuoles and apoptotic cells in the parotid gland and presence of vacuoles and disorganization of mucous acinus in the submandibular gland in the PS group. The expression of interleukins 6, 10 and TNF-ɑ was differentially expressed in the PS and R groups both in the parotid and submandibular glands. Apoptosis was triggered in both salivary glands, being in the submandibular gland in a more intense way, because it was detected an increase not only in the activated caspase-3 expression but also in the cytochrome C. The cellular proliferation was also detected by means of Ki-67 immunoexpression in the R groups of the two salivary glands. In short, sleep deprivation is able to trigger an inflammatory process, as well as activate apoptosis in the major salivary glands of rats.
Descrição
Citação
SOUZA, Ana Carolina Flygare. Atividade inflamatória e apoptótica em glândulas salivares de ratos induzidas pela privação de sono paradoxal. 2021. 131 f. Tese (Doutorado Interdisciplinar em Ciências da Saúde) - Instituto de Saúde e Sociedade, Universidade Federal de São Paulo, Santos, 2021.