肾脏去神经对家兔动脉粥样硬化粘附分子的影响

发布时间：2018-03-31 23:26

  本文选题：动脉粥样硬化　切入点：肾脏去神经　出处：《重庆医科大学》2015年硕士论文

【摘要】：背景：随着人口老龄化的加速,动脉粥样硬化(Atherosclerosis, AS)在人群中的发病率越来越高,可导致冠心病、脑卒中及其他外周器官功能障碍等疾病。目前其发病机制中的炎症学说逐渐受到人们的重视,其中单核细胞趋化蛋白-1(monocyte chemotactic protein-1, MCP-1)、细胞间粘附分子-1(intercellular adhesion molecule-1,ICAM-1)、血管细胞间粘附分子-1(vascular intercellular adhesion molecules-1,VCAM-1)和血小板内皮细胞粘附分子-1(platelet endothelial cell adhesion molecule-1, PEC AM-1)等粘附分子和动脉粥样硬化密切相关,促进了动脉粥样硬化的发生、发展过程。有研究发现,交感神经系统在调节肾素血管紧张素醛固酮系统(renin-angiotensin-aldosterone system, RAAS)方面发挥着重要的作用,交感神经过度激活,进一步激活RAAS系统,使得肾素、血管紧张素Ⅱ (Angiotensin Ⅱ,Ang Ⅱ)大量生成。而AngⅡ在动脉粥样硬化的形成上扮演着重要的角色,可促进动脉粥样硬化的形成。目前肾脏去神经(renal denervation,RDN)在治疗顽固性高血压和改善心功能等方面取得了一些进展,而对动脉粥样硬化粘附分子的作用及机制尚不清楚。目的：探讨肾脏去神经对家兔动脉粥样硬化粘附分子的影响。方法：28只雄性新西兰白兔随机平均分为正常对照组(control)、肾脏去神经(RDN)+高脂组、假手术(sham)+高脂组、单纯高脂饮食(high-fat-diet, HFD)组。检测血浆中血脂、去甲肾上腺素(Norepinephrine,NE)和氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)浓度,免疫组化检测AngⅡ、MCP-1和PEC AM-1的表达；蛋白印迹(Western blot)检测ICAM-1和VCAM-1的表达；RT-PCR检测MCP-1、PECAM-1、ICAM-1和VCAM-1的]mRNA的表达。结果：术后RDN组NE水平低于sham组和HFD组(P0.05),其血浆甘油三酯(Triglyceride,TG)浓度低于HFD组(P0.05); RDN组血浆ox-LDL浓度、主动脉的AngⅡ和粘附分子表达较sham组和HFD组明显降低(P0.05),RDN组内膜／中膜比值较HFD组降低(P0.05)。结论：RDN可降低交感神经活性和TG浓度,下调粘附分子的表达,延缓动脉粥样硬化形成。
[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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