摘要
最近的证据表明,脑缺血再灌注损伤起着重要的作用,如阿尔茨海默氏病(AD)和其他神经退行性疾病的致病性疾病。氧化应激诱导的有毒的活性氧(ROS)在脑缺血再灌注(CIR)在神经退行性疾病中起着重要的作用。因为脑缺血再灌注诱导的氧化应激,作为活性氧的产生主要源,神经元的线粒体,细胞的能量代谢中心的经历严重损害。线粒体功能障碍的过程是通过脑缺血再灌注,可能为阿尔茨海默氏病的神经退行性疾病的老年人的途径加速。脑缺血再灌注损伤预防可能分流以减少中老年人阿尔茨海默型痴呆症的风险。在脑缺血再灌注化学使用的抗氧化剂是不适合作为血脑屏障(BBB)不允许进入分子从血液循环进入大脑。因此在大鼠脑线粒体区,L-抗坏血酸加载,聚乳酸纳米胶囊制备和口服评估纳米胶囊抗坏血酸(NAA)的作用对脑缺血再灌注诱导的氧化损伤。线粒体损伤的脂质过氧化和原位抗氧化酶状态的程度进行了评估。细胞色素C的水平(Cyt c)、环氧合酶2(COX-2)和诱导型一氧化氮合酶的测定。结果表明,相较于在自由抗坏血酸(AA)、纳米胶囊抗坏血酸(NAA)比较更好的发挥保护脑组织线粒体活性氧介导的氧化损伤的预防脑缺血再灌注损伤。
关键词: 抗氧化,血脑屏障,缺血再灌注,纳米胶囊,氧化应激,活性氧
Current Alzheimer Research
Title:Nanocapsulated Ascorbic Acid in Combating Cerebral Ischemia Reperfusion- Induced Oxidative Injury in Rat Brain
Volume: 13 Issue: 12
Author(s): Sibani Sarkar, Abhishek Mukherjee, Snehasikta Swarnakar, Nirmalendu Das
Affiliation:
关键词: 抗氧化,血脑屏障,缺血再灌注,纳米胶囊,氧化应激,活性氧
摘要: Recent evidences suggest that cerebral ischemia-reperfusion insult plays significant role in pathogenic diseases like Alzheimer’s disease (AD) and other neurodegenerative diseases. Toxic reactive oxygen species (ROS) generated by induced oxidative stress in the episodes of cerebral ischemia-reperfusion (CIR) plays major role in neurodegeneration. As the prime source of ROS generation, neuronal mitochondria, the cellular energy metabolic centre experience severe damage because of CIR-induced oxidative stress. The process of mitochondrial dysfunction is accelerated by CIR that may pave the pathway for neurodegeneration in AD among aged individuals. Prevention of CIR injury may be a shunt in order to minimize the risk of dementia of Alzheimer’s type in aged individuals. The use of chemical antioxidants in CIR is not suitable as the blood- brain barrier (BBB) doesn’t allow the entry of molecules from blood circulation into the brain. Thus L-ascorbic acid loaded polylactide nanocapsules were prepared and fed orally to assess the role of nanocapsulated ascorbic acid (NAA) against CIR induced oxidative injury in mitochondrial region of rat brains. Mitochondrial injury was assessed by the extent of lipid peroxidation and in situ antioxidant enzyme status. The levels of cytochrome c (cyt c), cyclooxygenase- 2 (COX-2) and iNOS were determined. Results showed that in comparison to free ascorbic acid (AA), NAA exerted better protection to the brain mitochondria by preventing oxidative damage in ROS mediated CIR injury.
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Sibani Sarkar, Abhishek Mukherjee, Snehasikta Swarnakar, Nirmalendu Das , Nanocapsulated Ascorbic Acid in Combating Cerebral Ischemia Reperfusion- Induced Oxidative Injury in Rat Brain, Current Alzheimer Research 2016; 13 (12) . https://dx.doi.org/10.2174/1567205013666160625082839
DOI https://dx.doi.org/10.2174/1567205013666160625082839 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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