褪黑素对大鼠局灶性脑缺血保护作用的研究
发布时间:2019-01-21 12:36
【摘要】: 目的:缺血性脑血管病是常见的一种导致神经元损伤的疾病,缺血过程中神经元损伤的病理生理机制比较复杂,可能包括自由基损伤、兴奋性氨基酸的毒性作用、炎症白细胞的损害、细胞内钙超载等多种因素。近几年的研究热点多集中在自由基氧化反应与炎症白细胞引起的继发性脑损伤两方面。褪黑素(melatonin, MT)是由松果体合成分泌的重要神经内分泌激素之一,是一种很重要的自由基清除剂,从而起到抗氧化的作用。另外有研究,MT能抑制缺血心肌中白细胞的浸润,能抑制二硝基苯磺酸引起的炎性结肠组织中白细胞的浸润,能否抑制缺血时脑组织中白细胞的浸润未见报道。本实验采用大鼠局灶性永久性脑缺血模型,采用HE、分光光度计、免疫组织化学、电镜等方法观察缺血后大脑的形态结构的变化及丙二醛(malondialdehyde, MDA)、髓过氧化物酶(myeloperoxidase, MPO)、细胞间黏附分子-1 (intercellular adhesion molecule-1, ICAM-1)、核因子-κB (nuclear factor-[kappa]B, NF-κB)的变化,并经过腹腔注射MT(在术前30分钟腹腔注射20mg/kg),观察MT对脑缺血性损伤时大脑的形态结构改变及MDA、MPO、ICAM-1、NF-κB表达的影响。 方法:采用SD大鼠72只,雌雄不拘,体重230到250克。用线栓法造成大脑中动脉栓塞制成脑缺血模型。实验分三组:正常对照组(Sham组)、缺血组(I组)、MT治疗组
[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).
【学位授予单位】:河北医科大学
【学位级别】:硕士
【学位授予年份】:2006
【分类号】:R363
本文编号:2412670
[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).
【学位授予单位】:河北医科大学
【学位级别】:硕士
【学位授予年份】:2006
【分类号】:R363
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