高血糖加重全脑缺血再灌注后缺血不敏感区神经元损伤  

Hyperglycemia increases neuron injury in the invulnerable regions under global brain ischemia/reperfusion in rats

作　　者：景丽[1] 张建忠[1] 马轶[1] 郭风英[1] 王一理[2] 

机构地区：[1]宁夏医科大学病理学教研室,银川750004 [2]西安交通大学生命科学与技术学院免疫病理研究室,西安710061

出　　处：《解剖学杂志》2011年第4期496-499,共4页Chinese Journal of Anatomy

基　　金：国家自然科学基金（30560044）

摘　　要：目的：探讨高血糖条件下脑缺血再灌注损伤加重的机制。方法：通过双侧颈总动脉结扎及放血法制备大鼠全脑缺血／再灌注模型，采用组织病理学、组织化学显色和末端脱氧核苷酸转移酶介导的dUTP原位切口末端标记（TUNEL）染色，对比观察注射性高血糖和糖尿病性高血糖大鼠神经元变性以及凋亡。结果：缺血敏感区额叶皮质和海马CA1区可见，各实验组在缺血15min，再灌注1、3、6h各时间点变性和凋亡神经元数量均多于假手术组（P〈0．01）。但高血糖组、糖尿病组在缺血15min，再灌注1、3、6h各时间点，变性和凋亡神经元的数目与正常血糖组接近。在缺血耐受区扣带皮质和海马CA3区，高血糖组和糖尿病组在缺血15min，再灌注1、3、6h各时间点，变性和凋亡神经元的数目多于正常血糖组（P〈0．05）。在糖尿病组和高血糖组之间，各时间点变性和凋亡神经元数量无差异。结论：不论是急性高血糖还是糖尿病性高血糖，均可加重暂时性全脑缺血再灌注所引起的神经元损伤，特别是在高血糖条件下，大鼠脑缺血不敏感区扣带皮质和海马CA3区变性及凋亡神经元增加。Objective： To explore the mechanism by which increases brain injury induced by ischemia/reperfusion under hyperglycemia. Methods： Rats with hyperglycemia injected glucose （hyperglycemia group）, hyperglycemia with experimental diabetes mellitus （diabetes group） were subjected to 15 min of global brain ischemia, and then reperfused for 1, 3 and 6 hours. Global brain ischemia and reperfusion was induced with the 2-common carotid arteries occlusion model with exsanguination and reinfusing the shed blood. The degeneration and apoptosis of neurons in the experimental rats were detected by means of histopathology, histoehemistry and TdT-mediated-dUTP nick end labeling （TUNEL） techniques. Results： In the vulnerable regions of frontal cortex and CA1 sector of hippocampus, the degeneration and apoptosis of neurons in the rats with ischemia for 15 minutes and reperfusion for 1, 3 and 6 hours were significantly higher than those of sham operated rats （P〈0. 01）. There were no significant difference found between the rats with hyperglycemia and the diabetes group, and the rats normoglycemia at all time points in the regions frontal cortex and CA1 area of hippocampus （P〉0.05）. In the cingulate cortex and CA3 of hippocampus, the degeneration and apoptosis of neurons in the rats with hyperglycmia and diabetes were significantly increased compared with those in rats with normoglycemia （P〈0. 05）. No significant difference was demonstrated between the hyperglycemia group and diabetes group. Conclusion： For acute hyperglycemia or diabetic ones, the hyper- glycemia may aggravate the neuronal injury after transient ischemia and reperfusion. An obviously increased neuronal degeneration and apoptosis could be induced by ischemia and reperfusion under hyperglycemia, especially in invulnerable regions of the cingulate cortex and CA3 of hippocampus.

关 键 词：脑缺血 再灌注 高血糖 糖尿病 神经元 凋亡 变性 大鼠 

分 类 号：R743.31[医药卫生—神经病学与精神病学]