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腎臟去神經(jīng)對家兔動脈粥樣硬化粘附分子的影響

發(fā)布時間:2018-03-31 23:26

  本文選題:動脈粥樣硬化 切入點:腎臟去神經(jīng) 出處:《重慶醫(yī)科大學》2015年碩士論文


【摘要】:背景:隨著人口老齡化的加速,動脈粥樣硬化(Atherosclerosis, AS)在人群中的發(fā)病率越來越高,可導致冠心病、腦卒中及其他外周器官功能障礙等疾病。目前其發(fā)病機制中的炎癥學說逐漸受到人們的重視,其中單核細胞趨化蛋白-1(monocyte chemotactic protein-1, MCP-1)、細胞間粘附分子-1(intercellular adhesion molecule-1,ICAM-1)、血管細胞間粘附分子-1(vascular intercellular adhesion molecules-1,VCAM-1)和血小板內(nèi)皮細胞粘附分子-1(platelet endothelial cell adhesion molecule-1, PEC AM-1)等粘附分子和動脈粥樣硬化密切相關(guān),促進了動脈粥樣硬化的發(fā)生、發(fā)展過程。有研究發(fā)現(xiàn),交感神經(jīng)系統(tǒng)在調(diào)節(jié)腎素血管緊張素醛固酮系統(tǒng)(renin-angiotensin-aldosterone system, RAAS)方面發(fā)揮著重要的作用,交感神經(jīng)過度激活,進一步激活RAAS系統(tǒng),使得腎素、血管緊張素Ⅱ (Angiotensin Ⅱ,Ang Ⅱ)大量生成。而AngⅡ在動脈粥樣硬化的形成上扮演著重要的角色,可促進動脈粥樣硬化的形成。目前腎臟去神經(jīng)(renal denervation,RDN)在治療頑固性高血壓和改善心功能等方面取得了一些進展,而對動脈粥樣硬化粘附分子的作用及機制尚不清楚。目的:探討腎臟去神經(jīng)對家兔動脈粥樣硬化粘附分子的影響。方法:28只雄性新西蘭白兔隨機平均分為正常對照組(control)、腎臟去神經(jīng)(RDN)+高脂組、假手術(shù)(sham)+高脂組、單純高脂飲食(high-fat-diet, HFD)組。檢測血漿中血脂、去甲腎上腺素(Norepinephrine,NE)和氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)濃度,免疫組化檢測AngⅡ、MCP-1和PEC AM-1的表達;蛋白印跡(Western blot)檢測ICAM-1和VCAM-1的表達;RT-PCR檢測MCP-1、PECAM-1、ICAM-1和VCAM-1的]mRNA的表達。結(jié)果:術(shù)后RDN組NE水平低于sham組和HFD組(P0.05),其血漿甘油三酯(Triglyceride,TG)濃度低于HFD組(P0.05); RDN組血漿ox-LDL濃度、主動脈的AngⅡ和粘附分子表達較sham組和HFD組明顯降低(P0.05),RDN組內(nèi)膜/中膜比值較HFD組降低(P0.05)。結(jié)論:RDN可降低交感神經(jīng)活性和TG濃度,下調(diào)粘附分子的表達,延緩動脈粥樣硬化形成。
[Abstract]:Background: with the acceleration of population aging, the incidence of Atherosclerosis (ASS) in the population is increasing, which can lead to coronary heart disease. Stroke and other diseases such as peripheral organ dysfunction. At present, people pay more and more attention to the theory of inflammation in the pathogenesis of cerebral apoplexy. Among them, monocyte chemotactic protein-1, MCP-1, intercellular adhesion molecule-1, intercellular intercellular molecule-1, intercellular intercellular adhesion (-1) and platelet endothelial cell adhesion molecule -1platelet endothelial cell adhesion molecule-1 (PEC AM-1) are closely related to atherosclerosis. It has been found that the sympathetic nervous system plays an important role in regulating renin-angiotensin-aldosterone system (RAASS). Sympathetic nerves are over-activated and further activate the RAAS system. So that renin, angiotensin 鈪,

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