摘要
目的通过对自发性2型糖尿病小鼠发病早期认知功能的研究,探讨糖尿病脑病的发病机制。方法利用自发性2型糖尿病动物模型KK-Ay小鼠,动态研究其认知功能的变化,并进行脑组织形态学观察。结果在Morris水迷宫实验中,糖尿病小鼠在发病6周时已出现轻度认知功能障碍,在发病12周时认知功能障碍明显加重,游出时间、游出距离显著长于正常对照鼠(P<0.01)。光镜和电镜都观察到糖尿病小鼠脑组织形态学的变化,以电镜下超微结构的变化为主。发病12周时海马及颞叶神经元固缩、深染,核膜凹陷,核内染色质溶解,核糖体解聚,线粒体退变,内容物呈絮状,未观察到毛细血管基底膜增厚,管腔狭窄等血管病变。结论KK-Ay小鼠可以作为研究糖尿病脑病的一种较好的动物模型;高血糖等代谢因素可引起认知障碍的发生。
Objective To study the pathogenic mechanisms of diabetic encephalopathy. Methods Using KK-Ay mouse as the non-insulin dependent diabetes mellitus （NIDDM） model and age-matched C57BL/6J mouse as normal control, their cognitive pedormance in Morris water maze and morphological change in brain has been observed respectively at 6 and 12 weeks after onset of diabetes mellitus. Results KK-Ay diabetic mouse begin to display moderate learning deficits in the Morris maze 6 weeks after onset of diabetes. The cognitive impairment become more significant at 12 weeks： the swimming time and distance of diabetic mouse is significantly longer than the control; the pathological change of brain tissue has been observed by electron microscopy and light microscopy. Condusion KK-Ay diabetic mouse can be used as an animal model to study the pathogenesis of diabetic encephalopathy. The hyperglycemia may lead to the cognitive impairment in diabetes.
出处
《首都医科大学学报》
CAS
2007年第1期75-77,共3页
Journal of Capital Medical University
关键词
糖尿病脑病
发病机制
KK-Ay糖尿病小鼠
认知障碍
diabetic encephalopathy
pathogenetic mechanism
KK-Ay diabetic mouse
cognitive impairment
