实验性超负荷血糖大鼠血脑屏障的超微结构变化

Ultrastructural study of blood-brain barrier in streptozocin-induced hyperglycemic rat

目的探讨糖尿病对血脑屏障(BBB)超微形态学及其内皮细胞ICAM-1表达的影响。方法采用44只SD大鼠尾静脉注射链脲霉素的方法,建立超负荷血糖模型。以透射电镜动态观察3d至8个月不同时程超负荷血糖条件下BBB超微结构的改变。结果超负荷血糖3d至2个月时,出现部分血脑屏障之内皮细胞、胶质细胞足突肿胀;3个月时出现明显的血脑屏障改变,整个毛细血管呈哑铃样、串珠样、动脉瘤样变形;6～8个月时改变继续加重,可见毛细血管管腔内微血栓,病变的血脑屏障周围,出现内皮细胞和神经细胞凋亡。实验中未见胶质细胞凋亡和神经细胞坏死。对照组无血脑屏障改变。结论实验提示超负荷血糖可造成血脑屏障发生明显的超微形态学异常,尤以长期作用更加明显。这可能是慢性糖尿病患者发生非梗塞性缺血缺氧性脑病的重要病理学基础。

Objective To investigate the effect of diabetes mellitus on ultrastructural morphology and ICAM-1 expression of blood-brain barrier(BBB).Methods Hyperglycemia model was made by intravenous injection of streptozocin in 44 SD rats. A dynamic observation of the ultrastructure of BBB was taken in SD rats with hyperglycemia for 3 days to 8 months by transmission electron microscopy.Results Swelling was slight in endothelium of BBB of rats with hyperglycemia for 3 days, became obvious and occurred in endfoot of astrocyte for 1 to 2 months, and some microthrombi appeared in cavity of capillary with various malformation and apoptosis was found in endothelium of BBB and neuron surrounding abnormal capillary for 3 to 8 months. There was no changes on BBB in controls.Conclusion Hyperglycemia could cause obvious ultrastructural changes of BBB, especially its long-term effects,which suggest that it could be pathological base of non-infraction ischemia-anoxia brain disease patient.