活性氧通过影响线粒体膜电位参与小鼠高血糖加重脑缺血性损伤  

Reactive oxygen species involved in hyperglycemia aggravating cerebral ischemia injury by affecting mitochondrial membrane potential in mice

作　　者：岳萌 孙世辉 张紫晶 高伟俊 马轶[1] Yue Meng;Sun Shihui;Zhang Zijing;Gao Weijun;Ma Yi(Department of Pathology,Basic Medical College,Ningxia Medical University,Yinchuan 750004;Chiping Second People's Hospital,LiaoCheng 252000;Department of Neurology,Tangdu Hospital,the Air Force Military Medical University,Xi'an 710038;Department of Anesthesiology,General Hospital of Ningxia Medical University,Yinchuan 750004;Department of Developmental Biology,Basic Medical College,Ningxia Medical University,Yinchuan 750004)

机构地区：[1]宁夏医科大学基础医学院病理系,银川750004 [2]茌平县第二人民医院,聊城252000 [3]空军军医大学唐都医院神经内科,西安710038 [4]宁夏医科大学总医院麻醉科,银川750004 [5]宁夏医科大学基础医学院发育生物学系,银川750004

出　　处：《神经解剖学杂志》2019年第1期35-40,共6页Chinese Journal of Neuroanatomy

基　　金：国家自然科学基金资助项目(81760240;81360196);宁夏高等学校一流学科建设(宁夏医科大学西部一流建设学科基础医学)资助项目(NXYLXK2017B07)

摘　　要：目的:探讨活性氧(ROS)参与高血糖加重脑缺血性损伤的可能机制。方法:采用链脲佐菌素(STZ)诱导联合大脑中动脉栓塞(MCAO)法建立小鼠高血糖脑缺血再灌注模型,于再灌注后5、24 h收集脑组织,通过神经行为学评分、TTC染色评价高血糖对脑缺血性损伤的影响,用ROS荧光探针-二氢乙啶(DHE)、JC-1分析活性氧和线粒体膜电位(△ψ)的变化情况。结果:与正常血糖脑缺血组相比,高血糖脑缺血组神经行为学评分与脑梗塞体积明显增加,活性氧产量于再灌注5和24 h明显增加,线粒体膜电位于再灌注24 h明显去极化。结论:高血糖可加重脑缺血性损伤,且活性氧可能通过影响线粒体膜电位参与高血糖加重脑缺血性损伤。Objective: To explore the possible mechanism of reactive oxygen species( ROS) involved in hyperglycemia aggravating cerebral ischemic injury. Methods: Establish hyperglycemia mouse of focal cerebral ischemia model by induction with streptozotocin( STZ) and middle cerebral artery occlusion( MCAO). Their brains were harvested after 5h and 24 h of reperfusion for subsequent experiments. We evaluated the effect of hyperglycemia on infarct volume after cerebral ischemia by Longa score and 2,3,5-triphenyltetrazolium chloride( TTC) staining. We analyzed ROS production by ROS fluorescent probes-Dihydroethidine( DHE) and mitochondrial membrane potential( △ψ) by JC-1.Results: Compared with the normoglycemia ischemia group,the neurobehavioral score of the hyperglycemia ischemia group was significantly increased,and the volume of cerebral infarction,the production of reactive oxygen species increased significantly at 5 h,24 h of reperfusion. The mitochondrial membrane potential of hyperglycemia ischemia group depolarized obviously at 24 h of reperfusion. Conclusion: Hyperglycemia can aggravate cerebral ischemic injury,andreactive oxygen species may participate in hyperglycemia exaggerated cerebral ischemic injury by affecting mitochondrial membrane potential.

关 键 词：高血糖 脑缺血再灌注损伤 活性氧 线粒体膜电位 小鼠 

分 类 号：R587.2[医药卫生—内分泌] R743[医药卫生—内科学]