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Effects of exercise on brain and peripheral inflammatory biomarkers induced by total sleep deprivation in rats.

Chennaoui M, Gomez-Merino D, Drogou C, Geoffroy H, Dispersyn G, Langrume C, Ciret S, Gallopin T, Sauvet F - J Inflamm (Lond) (2015)

Bottom Line: Physical exercise induces neuroprotection through anti-inflammatory effects and total sleep deprivation is reported an inflammatory process.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.

View Article: PubMed Central - PubMed

Affiliation: Département Neurosciences et contraintes opérationnelles, Institut de recherche biomédicale des armées, Brétigny-sur-Orge, France ; Université Paris Descartes, Sorbonne Paris Cité, EA7330 VIFASOM, Paris, France ; Armed Forces Biomedical Research Institute (IRBA), B.P.73, 91223 Brétigny-sur-Orge, Cedex France.

ABSTRACT

Background: Physical 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.

Methods: Four 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.

Results: Compared 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.

Conclusions: We 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.

No MeSH data available.


Schematic representation of the experimental protocol
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Fig1: Schematic representation of the experimental protocol

Mentions: The two groups of exercised rats were trained by running on a motorized treadmill for seven weeks. In order to minimize stress, the rats were progressively accustomed to the treadmill for one week (5 days, 10–15 min at a speed of 15 m/min). Animals reluctant to run during this training period were not used in the experiment. At the end of this period, the training program began: the rats were exercised 60 min each day, over a two-week period, at 18 m/min. The workload was then progressively increased until at the end of 5 weeks the rats were running at 25 m/min, 7 % grade, for 120 min per day and 5 days per week. This level of exercise remained stable during the final two weeks Fig. 1. During these 7 weeks, the rats were weighed three times a week. The rats belonging to the sedentary groups were placed daily in a new cage and also weighed three times a week [30].Fig. 1


Effects of exercise on brain and peripheral inflammatory biomarkers induced by total sleep deprivation in rats.

Chennaoui M, Gomez-Merino D, Drogou C, Geoffroy H, Dispersyn G, Langrume C, Ciret S, Gallopin T, Sauvet F - J Inflamm (Lond) (2015)

Schematic representation of the experimental protocol
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4588685&req=5

Fig1: Schematic representation of the experimental protocol
Mentions: The two groups of exercised rats were trained by running on a motorized treadmill for seven weeks. In order to minimize stress, the rats were progressively accustomed to the treadmill for one week (5 days, 10–15 min at a speed of 15 m/min). Animals reluctant to run during this training period were not used in the experiment. At the end of this period, the training program began: the rats were exercised 60 min each day, over a two-week period, at 18 m/min. The workload was then progressively increased until at the end of 5 weeks the rats were running at 25 m/min, 7 % grade, for 120 min per day and 5 days per week. This level of exercise remained stable during the final two weeks Fig. 1. During these 7 weeks, the rats were weighed three times a week. The rats belonging to the sedentary groups were placed daily in a new cage and also weighed three times a week [30].Fig. 1

Bottom Line: Physical exercise induces neuroprotection through anti-inflammatory effects and total sleep deprivation is reported an inflammatory process.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.

View Article: PubMed Central - PubMed

Affiliation: Département Neurosciences et contraintes opérationnelles, Institut de recherche biomédicale des armées, Brétigny-sur-Orge, France ; Université Paris Descartes, Sorbonne Paris Cité, EA7330 VIFASOM, Paris, France ; Armed Forces Biomedical Research Institute (IRBA), B.P.73, 91223 Brétigny-sur-Orge, Cedex France.

ABSTRACT

Background: Physical 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.

Methods: Four 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.

Results: Compared 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.

Conclusions: We 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.

No MeSH data available.