慢性缺血致血管性癡呆大鼠海馬線粒體生物動能機制研究
發(fā)布時間:2018-12-25 19:54
【摘要】:血管性癡呆(VD)是腦血管疾病導(dǎo)致的記憶、認(rèn)知功能障礙臨床綜合征,是繼阿爾茨海默。ˋD)之后第二常見的癡呆類型,同時也是老年人中最常見的癡呆類型。VD病人多表現(xiàn)為執(zhí)行能力下降及行為心理癥狀,,如淡漠、意志力喪失、失認(rèn)、焦慮、抑郁及自殺傾向等,病人的生存質(zhì)量嚴(yán)重下降。隨著我國進(jìn)入老齡化社會,血管性癡呆已成為學(xué)者們關(guān)注的熱點問題。隨著人們對VD發(fā)病機制研究的深入,線粒體功能障礙在VD發(fā)生中所起的作用受到越來越多的關(guān)注。本研究通過對血管性癡呆模型大鼠線粒體能量代謝過程中的相關(guān)變化進(jìn)行研究,探討血管性癡呆的線粒體生物動能機制。 本研究選取Wistar健康雄性大鼠132只,隨機分為假手術(shù)組及模型組,各組再分2個月組、3個月組及4個月組。應(yīng)用雙側(cè)頸總動脈分次結(jié)扎法建立血管性癡呆大鼠模型,分別于造模前后應(yīng)用Morris水迷宮進(jìn)行行為學(xué)評估。通過應(yīng)用紫外分光光度計技術(shù)檢測細(xì)胞色素C氧化酶活性;應(yīng)用Western Blot法檢測細(xì)胞色素C氧化酶Ⅳ亞基蛋白表達(dá)變化和丙酮酸脫氫酶A1亞基蛋白表達(dá)變化;應(yīng)用熒光分光光度計技術(shù)檢測線粒體呼吸態(tài)4H2O2產(chǎn)率及應(yīng)用磷光性氧探針檢測線粒體呼吸態(tài)3耗氧情況。結(jié)果表明通過雙側(cè)頸總動脈分次結(jié)扎的方法可以建立穩(wěn)定可靠的VD大鼠模型;VD大鼠海馬線粒體細(xì)胞色素C氧化酶活性減低;細(xì)胞色素C氧化酶Ⅳ亞基蛋白表達(dá)下降;丙酮酸脫氫酶A1亞基蛋白表達(dá)下降;呼吸態(tài)4H2O2產(chǎn)率增加;呼吸態(tài)3耗氧減少。血管性癡呆模型大鼠海馬線粒體能量代謝障礙,提示線粒體生物動能機制是血管性癡呆的發(fā)病機制之一。
[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
本文編號: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
本文編號:2391565
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