MITOCHONDRIAL BIOENERGETIC DEFICITS IN THE HIPPOCAMPI OF RATS WITH CHRONIC ISCHEMIA-INDUCED VASCULAR DEMENTIA

被引:56
作者
Du, J. [1 ]
Ma, M. [2 ]
Zhao, Q. [2 ]
Fang, L. [3 ]
Chang, J. [2 ]
Wang, Y. [4 ]
Fei, R. [4 ]
Song, X. [5 ]
机构
[1] Jilin Univ, China Japan Union Hosp, Dept Vasc Surg, Changchun 130021, Jilin Province, Peoples R China
[2] Jilin Univ, China Japan Union Hosp, Dept Neurol, Changchun 130033, Jilin Province, Peoples R China
[3] Second Hosp ChangChun, Dept Neurol, Changchun 130062, Jilin Province, Peoples R China
[4] Jilin Univ, Dept Cell Biol, Sch Basic Med Sci, Changchun 130021, Jilin Province, Peoples R China
[5] Jilin Univ, Sch Publ Hlth, Changchun 130021, Jilin Province, Peoples R China
关键词
vascular dementia; mitochondria; bioenergetic deficit; OXIDATIVE STRESS; ALZHEIMERS-DISEASE; WISTAR RATS; CELL-DEATH; DYSFUNCTION; IMPAIRMENT; INHIBITION; PREVALENCE; DAMAGE;
D O I
10.1016/j.neuroscience.2012.11.062
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Vascular dementia (VD), defined as a loss of memory and cognitive function resulting from vascular lesions in the brain, is the second-most-common cause of dementia in the elderly, after Alzheimer's disease. In recent years, research has focused on the pathogenesis of VD, and mitochondrial bioenergetic deficits have been suggested to contribute to VD onset. To further investigate the role of mitochondria in VD, we used a rat model of VD, which involved permanent bilateral occlusion of the common carotid arteries (with a 1-week interval between artery occlusion to avoid an abrupt reduction in cerebral blood flow) leading to chronic cerebral hypoperfusion. Prior to occlusion, male Wistar rats underwent 7 days of Morris water maze training. Only animals that could swim and passed the Morris water maze test were chosen for the study. After 5 days of Morris water maze training, mitochondria from the hippocampi of rats, which were randomly selected from animals that could complete the Morris water maze test, were isolated for functional assessment. Mitochondria isolated from the hippocampi of rats from the ischemia group had decreased pyruvate dehydrogenase protein levels, and increased oxidative stress, as manifested by increased hydrogen peroxide production. The ischemia group mitochondria also exhibited decreased respiration coupled to decreased expression and activity of the electron transport chain complex IV (cytochrome c oxidase). These results indicate that the mitochondrial oxidative metabolism is inhibited in the hippocampi of rats following chronic ischemia-induced VD. As the mitochondrial oxidative metabolism deficits, namely mitochondrial bioenergetic deficits directly affect the functions of neurons, it may contribute to VD onset. (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:345 / 352
页数:8
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