食欲素A减少急性脑缺血大鼠的睡眠与运动障碍和迟发性神经元损伤  

Orexin-A reduces disorder of sleep and motor function and delayed neuron injury in acute cerebral ischemic rats

作　　者：张辉芳 尹晓刚[1] 白银雪 Zhang Huifang;Yin Xiaogang;Bai Yinxue(Department of Neurology,The First Affiliated Hospital of Nanyang Medical College,Nanyang 473000,China)

机构地区：[1]南阳医学高等专科学校第一附属医院神经内科,南阳473000

出　　处：《中国组织化学与细胞化学杂志》2020年第6期524-528,533,共6页Chinese Journal of Histochemistry and Cytochemistry

摘　　要：目的探讨食欲素A(orexin-A,OX-A)对急性缺血性脑卒中(acute ischemic stroke,AIS)大鼠的迟发性神经元损伤、睡眠障碍和运动功能恢复的影响。方法用线栓法制作大鼠短暂性大脑中动脉闭塞模型,并于术后1d侧脑室内注射30μg/kg OX-A。注射后7d,用脑电-肌电图来评估大鼠睡眠功能,用转棒实验和爬梯实验评估大鼠运动功能,用Nissl染色、NeuN染色和Fluro-Jade C染色观察大鼠神经元病理学改变。结果AIS大鼠的快动眼(rapid eye movement,REM)睡眠入睡潜伏期增加,睡眠片段化,觉醒次数增加,REM和非快动眼(non-rapid eye movement,NREM)睡眠的数量减少,神经元损伤增加,运动能力降低。外源性OX-A能缓解AIS大鼠睡眠变化,减轻神经元损伤,促进运动能力恢复。结论OX-A可明显减轻AIS大鼠的迟发性神经元损伤并改善睡眠和促进运动恢复。Objective To investigate the effects of Orexin-A(OX-A)on delayed neuron injury,sleep disorder and motor function recovery in acute ischemic stroke(AIS)rats.Methods Rat transient middle cerebral artery occlusion(tMCAO)model was established by wire occlusion,followed by intracerebroventricular injection of 30μg/kg OX-A at 1st d after surgery.At 7th d after injection,the sleep function of rats was evaluated by EEG-EMG recording;the motor function of rats was evaluated by rotarod and run staircase test;the pathological changes of rat neurons were observed by Nissl staining,NeuN staining and Fluro-Jade C staining.Results AIS rats had increased latency to rapid eye movement(REM)sleep onset,sleep fragmentation,and increased number of wake epochs,as well as decreased the number of REM and non-REM(NREM)sleep epochs.AIS rats also had increased neuronal damage and reduced motor function.While all the changes descirbed above could be alleviated by treatment with OX-A.Conclusion OX-A can significantly alleviate delayed neuronal injury of AIS rats,improve sleep quality and promote motor recovery.

关 键 词：食欲素A 急性缺血性脑卒中 睡眠障碍 迟发性神经元损伤 

分 类 号：R743.3[医药卫生—神经病学与精神病学]