The aim of this study was to evaluate if paradoxical sleep deprivation is able to induce tissue degeneration, inflammatory activity and apoptosis in the submandibular gland of rats. A total of 24 male Wistar rats were distributed into 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 paradoxical sleep deprivation for 96 h and group 3-recovery (R; n = 8): the animals were submitted to sleep deprivation for 96 h, followed by a period of 96 h without any intervention. The following parameters were evaluated: histopathological analysis, immunohistochemistry for Ki-67, COX-2 and cleaved caspase-3 and gene expression of TNF-α, Interleukin 6 (IL-6), Interleukin 10 (IL-10) and cytochrome C by real-time PCR. The results pointed out cytoplasmic vacuoles and congested vessels in the parenchyma of submandibular gland the in PS and R groups. The expression of interleukins 6, 10 and TNF-ɑ was differentially expressed in the PS and R groups. Apoptosis was also triggered by means of increasing cleaved caspase-3 and cytochrome c expression. The cellular proliferation (Ki-67 index) was also positive in the R group. Taken together, our results demonstrate that sleep deprivation is capable of promoting tissue degeneration in the submandibular gland, as a result of inflammatory response and cellular death in rats.
Keywords: Apoptosis; Inflammation; Rat; Sleep deprivation; Submandibular gland.
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