CAJ | 학술논문

目的:探讨亚低温对全脑缺血性癫痫大鼠认知功能和海马synapsinⅠ表达及突触超微结构的影响.方法:48只SD大鼠随机分为对照组(NC)、假手术组(Sham)、常温癫痫组(NT)和亚低温癫痫组(HT). 采用胸部挤压法建立全脑缺血声源性癫痫模型,HT组在NT组的基础上给予亚低温干预.免疫组化观察癫痫后24 h、3 d和14 d海马synapsinⅠ的表达,分别用Morris水迷宫实验和电镜观察大鼠的认知功能和突触超微结构. 结果:与NC和Sham组比较,NT组大鼠的synapsinⅠ表达降低,逃避潜伏期延长,穿过平台数减少(P<0.05);突触减少,线粒体肿胀,前后膜不清,髓鞘断裂. 与NT组比较,HT组synapsinⅠ表达在24 h无差异,3 d和14 d增加(P<0.01),逃避潜伏期降低、穿过平台数增加(P<0.01);突触结构转清,界面增长,突触后致密物质增厚.结论:亚低温可上调synapsinⅠ表达并减轻突触结构损伤,改善全脑缺血性癫痫大鼠的认知功能.
목적:탐토아저온대전뇌결혈성전간대서인지공능화해마synapsinⅠ표체급돌촉초미결구적영향.방법:48지SD대서수궤분위대조조(NC)、가수술조(Sham)、상온전간조(NT)화아저온전간조(HT). 채용흉부제압법건립전뇌결혈성원성전간모형,HT조재NT조적기출상급여아저온간예.면역조화관찰전간후24 h、3 d화14 d해마synapsinⅠ적표체,분별용Morris수미궁실험화전경관찰대서적인지공능화돌촉초미결구. 결과:여NC화Sham조비교,NT조대서적synapsinⅠ표체강저,도피잠복기연장,천과평태수감소(P<0.05);돌촉감소,선립체종창,전후막불청,수초단렬. 여NT조비교,HT조synapsinⅠ표체재24 h무차이,3 d화14 d증가(P<0.01),도피잠복기강저、천과평태수증가(P<0.01);돌촉결구전청,계면증장,돌촉후치밀물질증후.결론:아저온가상조synapsinⅠ표체병감경돌촉결구손상,개선전뇌결혈성전간대서적인지공능.
Objective To study the effects of mild hypothermia on cognitive function , synapsinⅠexpression and synaptic ultrastructure of hippocampus in epileptic rats induced by global cerebral ischemia. Methods Forty-eight male SD rats were randomly divided into control (NC) group, sham-operated (Sham) group, normothermic epilepsy (NT) group and mild hypothermic epilepsy (HT) group. The model of postischemic audio-genetic seizure was established by chest compression. Hypothermia intervention was given to HT group. Immunocytochemistry was conducted to detect the expressions of synapsin I in hippocampus at days 1 , 3, 14. the synaptic ultrastructure and cognitive function were respectively observed by electron microscope and Morris water maze. Results Compared with NC and Sham group, the expression of synapsinI in NT group was decreased, the escape latency was prolonged and across platform number decreased (P < 0.05). The synapses were decreased in number, and mitochondria was viewed swelling, synaptic membranes unclear, myelin fractured. Compared with NT group, the expression of synapsinⅠin HT group had no obvious change in 24 h but was significantly increased in days 3 and 14 (P < 0.01); The escape latency was decreased and the number of cross platform increased (P < 0.01); Synaptic structure was clear, with interface growing and postsynaptic density thickened. Conclusion Mild hypothermia may improve the cognitive function of the epileptic rats induced by global cerebral ischemia by upregulating the expression of synapsinⅠand alleviating the damage of synaptic structure.