【摘要】： 目的:缺血性腦血管病是常見的一種導(dǎo)致神經(jīng)元損傷的疾病,缺血過程中神經(jīng)元損傷的病理生理機制比較復(fù)雜,可能包括自由基損傷、興奮性氨基酸的毒性作用、炎癥白細胞的損害、細胞內(nèi)鈣超載等多種因素。近幾年的研究熱點多集中在自由基氧化反應(yīng)與炎癥白細胞引起的繼發(fā)性腦損傷兩方面。褪黑素(melatonin, MT)是由松果體合成分泌的重要神經(jīng)內(nèi)分泌激素之一,是一種很重要的自由基清除劑,從而起到抗氧化的作用。另外有研究,MT能抑制缺血心肌中白細胞的浸潤,能抑制二硝基苯磺酸引起的炎性結(jié)腸組織中白細胞的浸潤,能否抑制缺血時腦組織中白細胞的浸潤未見報道。本實驗采用大鼠局灶性永久性腦缺血模型,采用HE、分光光度計、免疫組織化學(xué)、電鏡等方法觀察缺血后大腦的形態(tài)結(jié)構(gòu)的變化及丙二醛(malondialdehyde, MDA)、髓過氧化物酶(myeloperoxidase, MPO)、細胞間黏附分子-1 (intercellular adhesion molecule-1, ICAM-1)、核因子-κB (nuclear factor-[kappa]B, NF-κB)的變化,并經(jīng)過腹腔注射MT(在術(shù)前30分鐘腹腔注射20mg/kg),觀察MT對腦缺血性損傷時大腦的形態(tài)結(jié)構(gòu)改變及MDA、MPO、ICAM-1、NF-κB表達的影響。 方法:采用SD大鼠72只,雌雄不拘,體重230到250克。用線栓法造成大腦中動脈栓塞制成腦缺血模型。實驗分三組:正常對照組(Sham組)、缺血組(I組)、MT治療組
[Abstract]:Objective: ischemic cerebrovascular disease (ICVD) is a common disease causing neuronal injury. The pathophysiological mechanism of neuronal injury during ischemia is complicated, which may include free radical injury and excitatory amino acid toxicity. Inflammatory leukocyte damage, intracellular calcium overload and other factors. In recent years, the research focuses on free radical oxidation and secondary brain injury caused by inflammatory leukocytes. Melatonin (melatonin, MT) is one of the important neuroendocrine hormones synthesized and secreted from the pineal gland. It is a very important scavenger of free radicals and thus plays an antioxidant role. In addition, MT can inhibit the infiltration of leukocytes in ischemic myocardium and the infiltration of leukocytes in inflammatory colon tissue induced by dinitrobenzene sulfonic acid. It is not reported whether MT can inhibit the infiltration of leukocytes in brain tissues during ischemia. In this study, the rat model of focal permanent cerebral ischemia was used to observe the changes of cerebral morphology and (malondialdehyde, MDA), myeloperoxidase (myeloperoxidase,) after ischemia by HE, spectrophotometer, immunohistochemistry and electron microscope. The changes of MPO), intercellular adhesion molecule-1 (intercellular adhesion molecule-1, ICAM-1, nuclear factor- 魏 B (nuclear factor- [kappa] B, NF- 魏 B, and intraperitoneal injection of MT (20mg/kg 30 minutes before operation) were observed. To observe the effect of MT on the changes of brain morphology and the expression of MDA,MPO,ICAM-1,NF- 魏 B in ischemic brain injury. Methods: 72 SD rats, male and female, weighing 230 to 250g. Middle cerebral artery embolization was used to make cerebral ischemia model. The experiment was divided into three groups: normal control group (Sham group) and ischemic group (), MT treatment group I).
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2006
【分類號】：R363

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