Nor, Nur Syafiqah Mohmed
(2020)
Role of oxidative stress in rem sleep deprivation-induced endothelial dysfunction in rat model.
Masters thesis, Universiti Sains Malaysia.
Abstract
Sleep deprivation is associated with endothelial dysfunction, an early sign of
cardiovascular disease. The pathogenesis underlying endothelial dysfunction in sleep
deprivation remains poorly understood to date. The objective of this study was to
identify the possible factors involved in the mechanism of endothelial dysfunction in
sleep deprivation, in particular REM sleep phase. Only experiments for the first
objective were carried out in this study as a result of the Movement Control Order
(MCO) of the Federal Government of Malaysia due to the pandemic of coronavirus
disease (COVID-19). Eight (8) male Sprague-Dawley rats were equally divided into
four groups; free-moving control rats (FMC), 72-h REM sleep-deprived rats (REMsd),
tank control rats (TC) and sleep recovery for 72 hours after 72 hours of REM sleep
deprivation rats (SR). Rats were deprived of REM sleep using the inverted flowerpot
technique. There was no significant differences in the levels of food consumption, body
weight gain and systolic blood pressure between the groups. The levels of protein
expression of endothelial nitric oxide synthase (eNOS) and phosphorylated eNOS (peNOS),
and the levels of oxidative stress markers in the aorta; total antioxidant
capacity (TAC), catalase (CAT), and superoxide dismutase (SOD) were not measured
due to time constraints. Based on the assumption that REM sleep deprivation induced
endothelial dysfunction, it is expected that there will be a significant decrease in the
levels of p-eNOS in the REMsd group compared to other groups. Oxidative stress has
been postulated as a possible factor in the mechanism of endothelial dysfunction, thus
a significant decrease in the levels of antioxidants is expected to occur in aortic tissue.
In conclusion, it is postulated that REM sleep deprivation is associated with
endothelial dysfunction that may be induced by oxidative stress
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