甲基莲心碱对光化学诱导大鼠脑缺血损害的保护作用  

Protective effect of neferine on ischemic brain damage induced by photochemistry

作　　者：刘剑萍[1] 唐伟军[1] 吴俊[1] 卢平[1] 陈雁冰[1] 

机构地区：[1]郴州医专心脑血管疾病研究所

出　　处：《中国临床药学杂志》2002年第5期267-269,共3页Chinese Journal of Clinical Pharmacy

摘　　要：目的 :探讨甲基莲心碱对脑缺血的保护作用。方法 :应用光化学诱导大鼠大脑中动脉栓塞 (MCAO)模型 ,观察预防性使用甲基莲心碱对脑梗死范围 ,梗死区脑组织H2 O ,Ca2 + ,NO ,丙二醛 (MDA)含量以及超氧化物歧化酶 (SOD)活力的影响。结果 :光化学反应 6h后 ,脑梗死范围占同侧半球体积的 (2 0 9+4 3) % ,梗死区脑组织Ca2 + ,H2 O ,MDA含量增高而NO水平和SOD活力下降。预防性给予甲基莲心碱可缩小脑梗死面积 ,同时增加梗死区脑组织NO水平和SOD活力 ,降低Ca2 + ,H2 O ,MDA含量。结论 :甲基莲心碱具有减轻大鼠脑缺血的作用 ,其机制可能与对抗脑缺血时NO ,Ca2 + 的病理性改变有关。AIM: To study the effects of neferine (Nef) on ischemic brain damage induced by photochemistry in rats. METHODS: The rat model of middle cerebral artery occlusion (MCAO) was induced by photochemistry and the contents of H 2O, Ca 2+ and MDA as well as NO level and superoxide dismutase (SOD) activity were measured. RESULTS: Six hours after MACO induced by photochemistry, cerebral ischemia was formed, NO level and SOD activity were decreased. However, the contents of H 2O,Ca 2+ and MDA were increased. Nef reduced the ischemic areas of brain, decreased contents of Ca 2+ , H 2O and MDA. Furthermore, Nef also increased NO level and SOD activity of brain. CONCLUSION: Decrease of NO level and Ca 2+ overload are important factors leading to ischemic brain damage. Nef can be used to protect ischemic brain damage by influencing pathological changes of NO and Ca 2+ level.

关 键 词：一氧化氮 光化学反应 脑缺血 甲基莲心碱 

分 类 号：R965[医药卫生—药理学]