慢性缺血致血管性痴呆大鼠海马线粒体生物动能机制研究
发布时间：2018-12-25 19:54
【摘要】：血管性痴呆（VD）是脑血管疾病导致的记忆、认知功能障碍临床综合征，是继阿尔茨海默病（AD）之后第二常见的痴呆类型，同时也是老年人中最常见的痴呆类型。VD病人多表现为执行能力下降及行为心理症状，，如淡漠、意志力丧失、失认、焦虑、抑郁及自杀倾向等,病人的生存质量严重下降。随着我国进入老龄化社会，血管性痴呆已成为学者们关注的热点问题。随着人们对VD发病机制研究的深入，线粒体功能障碍在VD发生中所起的作用受到越来越多的关注。本研究通过对血管性痴呆模型大鼠线粒体能量代谢过程中的相关变化进行研究，探讨血管性痴呆的线粒体生物动能机制。 本研究选取Wistar健康雄性大鼠132只，随机分为假手术组及模型组，各组再分2个月组、3个月组及4个月组。应用双侧颈总动脉分次结扎法建立血管性痴呆大鼠模型，分别于造模前后应用Morris水迷宫进行行为学评估。通过应用紫外分光光度计技术检测细胞色素C氧化酶活性；应用Western Blot法检测细胞色素C氧化酶Ⅳ亚基蛋白表达变化和丙酮酸脱氢酶A1亚基蛋白表达变化；应用荧光分光光度计技术检测线粒体呼吸态4H2O2产率及应用磷光性氧探针检测线粒体呼吸态3耗氧情况。结果表明通过双侧颈总动脉分次结扎的方法可以建立稳定可靠的VD大鼠模型；VD大鼠海马线粒体细胞色素C氧化酶活性减低；细胞色素C氧化酶Ⅳ亚基蛋白表达下降；丙酮酸脱氢酶A1亚基蛋白表达下降；呼吸态4H2O2产率增加；呼吸态3耗氧减少。血管性痴呆模型大鼠海马线粒体能量代谢障碍，提示线粒体生物动能机制是血管性痴呆的发病机制之一。
[Abstract]:Vascular dementia (VD) is the second most common type of dementia after Alzheimer's disease (AD), which is a clinical syndrome of memory and cognitive impairment caused by cerebrovascular disease. At the same time, it is the most common type of dementia in the elderly. Most of the VD patients have decreased executive ability and behavioral and psychological symptoms, such as apathy, loss of willpower, agnosia, anxiety, depression and suicidal tendency, etc. With China's aging society, vascular dementia has become a hot issue that scholars pay attention to. With the further study of the pathogenesis of VD, more and more attention has been paid to the role of mitochondrial dysfunction in the pathogenesis of VD. In this study, we studied the changes of mitochondrial energy metabolism in vascular dementia model rats, and explored the mechanism of mitochondrial kinetic energy of vascular dementia. In this study, 132 healthy male Wistar rats were randomly divided into sham operation group and model group. Each group was divided into 2 months group, 3 months group and 4 month group. The rat models of vascular dementia were established by bilateral common carotid artery ligation. Morris water maze was used to evaluate the behavior before and after the establishment of the model. The activity of cytochrome C oxidase was detected by ultraviolet spectrophotometer, the expression of cytochrome C oxidase 鈪
本文编号：2391565
[Abstract]:Vascular dementia (VD) is the second most common type of dementia after Alzheimer's disease (AD), which is a clinical syndrome of memory and cognitive impairment caused by cerebrovascular disease. At the same time, it is the most common type of dementia in the elderly. Most of the VD patients have decreased executive ability and behavioral and psychological symptoms, such as apathy, loss of willpower, agnosia, anxiety, depression and suicidal tendency, etc. With China's aging society, vascular dementia has become a hot issue that scholars pay attention to. With the further study of the pathogenesis of VD, more and more attention has been paid to the role of mitochondrial dysfunction in the pathogenesis of VD. In this study, we studied the changes of mitochondrial energy metabolism in vascular dementia model rats, and explored the mechanism of mitochondrial kinetic energy of vascular dementia. In this study, 132 healthy male Wistar rats were randomly divided into sham operation group and model group. Each group was divided into 2 months group, 3 months group and 4 month group. The rat models of vascular dementia were established by bilateral common carotid artery ligation. Morris water maze was used to evaluate the behavior before and after the establishment of the model. The activity of cytochrome C oxidase was detected by ultraviolet spectrophotometer, the expression of cytochrome C oxidase 鈪
本文编号：2391565
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