Inflammatory activity and apoptosis are associated with tissue degeneration in the submandibular gland of rats submitted to paradoxical sleep deprivation

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.