大鼠慢性脑灌注不足诱导神经退行性变中氧化还原状态的研究。
Investigation of redox status in chronic cerebral hypoperfusion-induced neurodegeneration in rats.
作者信息
Saxena Anil Kumar, Abdul-Majeed Saif Saad, Gurtu Sunil, Mohamed Wael M Y
机构信息
Department of Basic Medical Sciences, Faculty of Medicine, IIUM, 25200 Kuantan, Malaysia.
Department of Life Sciences, International Medical University, Bukit Jalil, 5700 Kuala Lumpur, Malaysia.
出版信息
Appl Transl Genom. 2015 Jun 20;5:30-2. doi: 10.1016/j.atg.2015.05.004. eCollection 2015 Jun 1.
Abstract
Aging related reduction in cerebral blood flow (CBF) has been linked with neurodegenerative disorders including Alzheimer's disease and dementia. Experimentally, a condition of chronic cerebral hypoperfusion due to reduced CBF can be induced by permanent bilateral occlusion of common carotid arteries (2-vessel occlusion, 2VO) in rats. Since oxidative stress, leading to neuronal apoptosis and death, is one of the mechanisms, which is thought to play a significant role in chronic degenerative neurological disorders, the present study was planned to assess the ROS status by measuring the levels of anti-oxidant enzymes that might occur during chronic cerebral hypoperfusion. Antioxidant enzymes namely glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase were measured in the brain tissue at eight weeks of 2VO induction in rats. Results show significantly elevated levels of GPx, SOD, and catalase enzymes as compared with the control group. It is possible that compensatory rise in antioxidant enzymes occurs in response to increased oxidative stress following ischemic insult.
摘要
与衰老相关的脑血流量（CBF）减少与包括阿尔茨海默病和痴呆症在内的神经退行性疾病有关。在实验中，大鼠永久性双侧颈总动脉闭塞（双血管闭塞，2VO）可诱导因CBF减少导致的慢性脑灌注不足状态。由于氧化应激导致神经元凋亡和死亡，是被认为在慢性退行性神经疾病中起重要作用的机制之一，因此本研究计划通过测量慢性脑灌注不足期间可能出现的抗氧化酶水平来评估活性氧（ROS）状态。在大鼠2VO诱导八周时，测量脑组织中的抗氧化酶，即谷胱甘肽过氧化物酶（GPx）、超氧化物歧化酶（SOD）和过氧化氢酶。结果显示，与对照组相比，GPx、SOD和过氧化氢酶水平显著升高。抗氧化酶的代偿性升高可能是对缺血性损伤后氧化应激增加的反应。
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