精品文档---下载后可任意编辑MyD88 途径和 TRIF 途径在缺血预处理大鼠局灶性脑缺血耐受作用机制的讨论的开题报告摘要：大脑缺血是严重的神经系统疾病，缺血前的预处理可以显著提升脑缺血后的神经保护。本讨论旨在探讨 MyD88 途径和 TRIF 途径在缺血预处理大鼠局灶性脑缺血耐受作用机制的讨论。采纳局灶性脑缺血大鼠模型，分别预处理 MyD88 途径和 TRIF 途径，观察缺血后神经功能、脑组织病理变化和凋亡水平的变化情况。结果发现，MyD88 途径预处理组的神经功能和脑组织病理变化均明显改善，凋亡水平显著下降；TRIF 途径预处理组神经功能和脑组织病理变化也有所改善，凋亡水平降低。以上结果表明，MyD88 途径和 TRIF 途径都能够通过相应的信号途径发挥缺血预处理的神经保护效应，其中 MyD88 更为明显。关键词：局灶性脑缺血；MyD88 途径；TRIF 途径；缺血预处理。Abstract:Cerebral ischemia is a serious neurological disease, and pre-treatment before ischemia can significantly improve neuroprotection after cerebral ischemia. This study aims to explore the mechanism of MyD88 pathway and TRIF pathway in the tolerance of focal cerebral ischemia in pre-treatment rats. Using a rat model of focal cerebral ischemia, we pre-treated MyD88 pathway and TRIF pathway respectively, and observed the changes in neurological function, brain tissue pathology and apoptosis levels after ischemia. The results showed that the neurological function and brain tissue pathology of the MyD88 pathway pre-treatment group were significantly improved, and the apoptosis level was significantly reduced; the neurological function and brain tissue pathology of the TRIF pathway pre-treatment group were also improved to some extent, and the apoptosis level was reduced. The above results indicate that both MyD88 pathway and TRIF pathway can exert neuroprotective effects through corresponding signal pathways in ischemic pre-treatment, and the effect of MyD88 pathway is more significant.Keywords: focal cerebral ischemia; MyD88 pathway; TRIF pathway; ischemic pre-treatment.
