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机构地区:[1]泰山医学院药理教研室,山东泰安271000 [2]泰山慢性病医院,山东泰安271000
出 处:《中成药》2001年第10期729-731,共3页Chinese Traditional Patent Medicine
基 金:山东省卫生厅计划课题 (No .188)
摘 要:目的 :研究不同剂量的三七皂苷 (PNS)对局灶脑缺血所造成的神经功能障碍及超微结构的影响作用。方法 :Wistar大鼠 3 5只 ,随机分组。按照文献制备可逆性大脑中动脉梗塞 (MCAO)性脑缺血模型。利用诱发电位肌电图测试仪 ,测各组MCAO前后SEP的变化 ,脑皮质NO、SOD含量 ,及电镜超微结构的改变 ,观察三七皂苷对MCAO性脑损伤的保护作用。结果 :PNS 4 0 0mg·kg-1、2 0 0mg·kg-1均能明显缩短MCAO后SEP潜伏期时间 ,降低缺血区NO含量 ,增加SOD活性。与对照组比较有显著统计学意义 (P <0 .0 1) ,超微结构研究显示 ,三七皂苷能明显减轻缺血脑组织细胞损伤及神经元的坏死程度。结论 :三七皂苷能减轻局灶性脑缺血所造成的神经功能障碍。作用机理可能与增加SOD活性 ,降低脑NO含量 ,阻止Ca2 +内流有关。Objective: To study the effect of notoginsenoside in various doses on local ischemic neurotic dysfunction and the ultrastructure. Methods: 35 Wistar rats were divided at random. The reversible middle cerebral artery occlusion (MCAO) model was made according to the assessment of the literature. The changes of SEP contents of cerebral cortex NO and SOD, and the changes of the ultrastrcture were recorded by evoked potential electrograph before and after MCAO. Results: notoginsenoside 200mg·kg -1 and 400mg·kg -1 could remarkably alter MCAO, shorten the latent period, improve the dysfuntion induced by MCAO, lower the concentration of NO and enhance the activity of SOD. The differential value in MCAO group was statistically remarkable ( P <0.01). The ultrastructure indicated that notoginsenoside could remarkably lessen cerebral ischenic damage and the neurotic necrosis. Conclusion: notoginsenoside can play a significant role in improving local ischemic neurotic dysfunction, and the mechanism of the action probably lies in antioxidant free radicals, the lowering of cerebral NO level and the blocking of the inflow of Ca 2+ .
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