【摘要】 目的:研究三七皂苷保护缺血脑组织中神经元的机制。方法:应用免疫细胞化学SP法和计算机图象分析系统观察三七皂苷(7mg.kg-1,i.m) 对不同缺血时间(4,12和24h)老龄大鼠大脑皮质、海马与尾壳核内神经元型一氧化氮合酶(nNOS)表达丰度和病理组织学变化的影响。结果:单侧结扎颈总动脉可使大脑皮层、海马与尾壳核内nNOS的表达丰度显著下降,部分神经元出现空泡样变性。预先注射三七皂苷可有效阻止大脑皮质、海马与尾壳核内nNOS表达丰度的下降,并减少这些区域的病理学改变。结论:三七皂苷可促进缺血早期脑组织表达nNOS,并由此对神经元发挥保护作用。更多还原

【Abstract】 OBJECTIVE:To investigate and consider the protective mechanism of notoginsenoside on neurons in ischemic brains. METHODS: Immnocytochemistry and computer image analysis system were employed to detect the expression abundance of neuronal nitric oxide synthase(nNOS) in cerebral cortex, hippocampus, and caudate puta-men nuclei from a Rat model of incomplete cerebral ischemia at different timepoints of unilateral common carotid artery occlusion(4, 12, and 24hJ with i.m. injection of notoginsenoside 4h prior to ischemic model replication. At the same time, histopathological changes of neuronal damage were evaluated by utilizing the H & E staining procedure. RESULTS:The expression abundance of nNOS in cerebral cortex, hippocampus, and caudate putamen nuclei from the rats with unilateral common carotid artery being ligated decreased. Some neurons on the slices prepared from isdemic cerebral cortex, hippocampus, and caudate putamen nuclei appeared to be vacuolar degeneration. Pretreatment decreases of nNOS and reduce the extent of neuronal damage induced by ischemia. CONCLUSION: Notoginsenoside may play a newroprotective role in incomplete cerebral ischemia through upregulating the expression of nNOS in cerebral cortex. hippocampus, and caudate putamen nuclei.更多还原