■睡眠不足可能会导致神经炎症,这可能会增加神经炎症标志物,如神经元特异性烯醇化酶(NSE),肌酸激酶-脑部分(CK-BB),血液中的乳酸脱氢酶脑级分(LDH-BB)。因此,我们评估了REM睡眠剥夺和恢复对这些标志物的影响.
■将24只成年雄性SpragueDawley大鼠分组为对照组,环境控制,REM睡眠剥夺,24小时睡眠恢复。大鼠被剥夺睡眠72小时并恢复24小时。NSE,CK-BB,采用ELISA法测定血清中LDH-BB水平。
■血清NSE,CK-BB,与对照组相比,72小时睡眠剥夺组的LDH-BB显著升高(p<0.01)。经过24小时的睡眠恢复,NSE的水平,CK-BB,和LDH-BB与对照组相当(p>0.05)。
■REM睡眠剥夺增加血清NSE,CK-BB,LDH-BB,这可能是神经损伤造成的.然而,24小时的睡眠恢复恢复了这些标记。
UNASSIGNED: Sleep loss may contribute to neuroinflammation, which might increase neuroinflammatory markers such as neuron-specific enolase (NSE), creatine kinase-brain fraction (CK-BB), lactate dehydrogenase brain fraction (LDH-BB) in blood. Hence, we evaluated the effect of REM sleep deprivation and recovery on these markers.
UNASSIGNED: Twenty-four adult male Sprague Dawley rats were grouped as control, environmental control, REM sleep deprivation, and 24 hour sleep recovery. The rats were sleep deprived for 72 hours and recovered for 24 hours. NSE, CK-BB, and LDH-BB levels in serum were measured using ELISA.
UNASSIGNED: The serum NSE, CK-BB, and LDH-BB were significantly higher in 72 hour sleep deprived group compared to control (p<0.01). After 24 hours of sleep recovery, the levels of NSE, CK-BB, and LDH-BB were comparable to control (p>0.05).
UNASSIGNED: REM sleep deprivation increased serum NSE, CK-BB, and LDH-BB, which might be due to neural damage. However, 24 hours of sleep recovery restored these markers.