摘要
目的探讨大鼠低血糖后不同升高血糖水平对大鼠脑损伤的影响及脑损伤产生的机制。方法将4月龄SD雄性大鼠36只随机分为模型组(24只)、空白对照组(6只)、假手术组(6只)。参照Sang Won Suh等方法制作低血糖大鼠模型,将模型组大鼠按血糖升高水平再分为1～3mmol/L、3～6mmol/L、6～9mmol/L和>9mmol/L亚组。空白对照组为不作任何处理的正常大鼠,假手术组即正常血糖组。采用HE染色方法观察造模术后7d大鼠海马CA1区、齿状回(dentate gyrus,DG)和皮层神经元坏死情况,采用透射电镜观察造模术后7d大鼠海马神经元超微结构变化,采用阴离子荧光探针检测灌注结束时海马活性氧自由基(reactive oxygen species,ROS)的产生。结果 (1)HE染色:与空白对照组比较,假手术组、1～3mmol/L组大鼠海马CA1、DG及颞叶皮层细胞坏死数变化无统计学差异(P>0.05),3～6mmol/L组、6～9mmol/L组、>9mmol/L组海马CA1、DG及颞叶皮层细胞坏死数较假手术组明显增加(P<0.05,P<0.01)。(2)透射电镜:与假手术组比较,各模型组海马细胞均有不同程度损伤,其中>9mmol/L组损伤程度最重,1～3mmol/L组损伤程度最轻。(3)ROS检测:与假手术组比较,1～3mmol/L组、3～6mmol/L组、6～9mmol/L组、>9mmol/L组海马CA1区和DG区荧光信号均明显增加(P<0.05,P<0.01)。与1～3mmol/L组比较,3～6mmol/L组、6～9mmol/L组和>9mmol/L组海马CA1区和DG区荧光信号均升高(P<0.01),而3～6mmol/L组和6～9mmol/L组相比则无统计学差异(P>0.05)。结论大鼠严重低血糖后升高血糖水平过高会促进ROS的产生并且加重脑损伤。
Objective To explore the influence of different blood glucose rising levels on brain injury in rats after hypoglycemia and its mechanism. Methods A total of 36 SD rats （age： 4 months, male） were randomly divided into 3 groups： the experimental group （24 rats）, the blank control group （6 rats） and the sham surgery group （6 rats）. Hypoglycemia animal models were made according to the method used by Sang Won Suh et al. According to the blood glucose levels after reperfusion, 24 rats from the experimental group were sub-divided into 4 subgroups： 1-3 retool/L, 3 6 mmol/L, 6-9 mmol/L and; 9 mmol/L. No treatment was adopted in the blank group. The blood glucose of the sham group was normal. HE staining was used to detect the neurons necrosis in hippoeampal CA1, dentate gyrus （DG） and cortex 7 days after reperfusion. Electron microscope was used to observe the ultrastructural pathology of hippocampus 7 days after reperfusion. Dihydroethidium was used to evaluate the production of reactive oxygen species （ROS） after reperfusion. Results （1） HE staining： The number of necrotic neurons in hippocampus CA1, DG and temporal lobe cortex showed no statistically difference between the sham group and 1-3 mmol/L group and the blank group （P〉0.05）. Compared to the sham group, the number of necrotic neurons in the 3-6 mmol/L group, 6-9 mmol/L group and 〉9 mmol/L group showed significant increase （P〈0.05, P;0.0]）. （2） Electron microscope： Compared with the sham group, it caused neuron injury in 4 experiment groups, especially in ）9 mmol/L group, and only caused slightly neuron injury in 1-3 mmol/L group. （3） ROS detection： Et signal showed an obvious increase from the 4 experiment groups （1-3 mmol/L group, 3-6 mmol/L group, 6-9 mmol/L group, ;9 mmol/ L group ） , compared with the sham group （P;0.05, P;0.01）. Compared with the 1-3 mmol/L group, there were statistically significant differences of the fluorescence signal in the 3-6 mmol/L group, 6-9 mmol/L group and
出处
《中国神经免疫学和神经病学杂志》
CAS
北大核心
2013年第5期322-326,共5页
Chinese Journal of Neuroimmunology and Neurology
基金
国家自然科学基金资助项目(30971032)
关键词
低血糖症
脑损伤
海马
hypoglycemia
brain injury
hippocampus
