褪黑素對(duì)大鼠局灶性腦缺血保護(hù)作用的研究
[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(jí)別】:碩士
【學(xué)位授予年份】:2006
【分類號(hào)】:R363
【參考文獻(xiàn)】
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