Abstract
BackgroundPhysical exercise induces neuroprotection through anti-inflammatory effects and total sleep deprivation is reported an inflammatory process. We examined whether 7 weeks of exercise training attenuates markers of inflammation during total sleep deprivation (24-h wakefulness) in the rat brain and periphery.MethodsFour groups of 10 rats were investigated: Sedentary control, Sedentary sleep-deprived, Exercised control, and Exercised sleep-deprived. Sleep deprivation and exercise training were induced using slowly rotating wheels and a motorized treadmill. We examined mRNA expression of pro-inflammatory (IL-1β, TNF-α, and IL-6) cytokine-related genes using real-time PCR, and protein levels in the hippocampus and frontal cortex, as well as circulating concentrations.ResultsCompared to Sedentary control rats, hippocampal and cortical IL-1β mRNA expressions in Sedentary sleep-deprived rats were up-regulated (p < 0.05 and p < 0.01 respectively). At the protein level, hippocampal IL-1β and TNF-α and cortical IL-6 contents were higher in Sedentary sleep-deprived rats (p < 0.001, p < 0.05, p < 0.05, respectively). Peripherally, TNF-α, IL-6 and norepinephrine concentrations were higher in Sedentary sleep-deprived rats compared to Sedentary control (p < 0.01, p < 0.001, p < 0.01, respectively). Exercise training reduced the sleep deprivation-induced hippocampal IL-1β increases (mRNA expression and protein content) (p < 0.05 and p < 0.001), and TNF-α content (p < 0.001). At the periphery, exercise reduced sleep deprivation-induced increase of IL-6 concentration (p < 0.05) without effect on TNF-α and norepinephrine.ConclusionsWe demonstrate that a 7-week exercise training program before acute total sleep deprivation prevents pro-inflammatory responses in the rat hippocampus, particularly the IL-1β cytokine at the gene expression level and protein content.
Highlights
Physical exercise induces neuroprotection through anti-inflammatory effects and total sleep deprivation is reported an inflammatory process
Body and adrenal gland weights The body weight gain of Sedentary sleep-deprived rats was not statistically different compared to Sedentary control (270 ± 11 g vs 293 ± 5 g), while Exercised sleep-deprived rats was lower than Exercised control [244 ± 3 g vs 296 ± 11 g, F(3,33) = 8.17, p < 0.01]
Quantitative analysis of cytokines and Toll-like receptor (TLR)-4 gene expression in brain areas Hippocampus The IL-1β mRNA expression was higher in Sedentary sleep-deprived rats compared to Sedentary control rats [F(3,28) = 3.17, p < 0.05]
Summary
Physical exercise induces neuroprotection through anti-inflammatory effects and total sleep deprivation is reported an inflammatory process. Irwin et al [10, 11] demonstrated that sleep loss induced monocyte production and transcription of IL-6 and TNF-α RNA messenger under the influence of the nuclear factor kappa-beta (NF)-κB transcription control pathway that play a key role in controlling cellular expression of proinflammatory genes. For this author, Toll-like receptors (TLRs) TLR-4 play a role in the activation of NF-κB [12], and we showed increase in whole-blood TLR-4 mRNA in men during sleep loss [13]. In elderly men (e.g., large study of 4,252 subjects, 60 to 79 years old), Wannamethee et al [26] observed that several hemostatic and inflammatory variables were dose-dependently and inversely associated with current physical activity
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