延胡索乙素对大鼠局灶性脑缺血再灌注损伤的保护作用  

Protective effects of dl-tetrahydropalmatine on focal brain ischemia-reperfusion injury in rats

作　　者：梁健[1] 郑平香[1] 梁京生 

机构地区：[1]广州医学院药理学教研室,广州510182

出　　处：《中国药理学通报》1998年第5期413-415,共3页Chinese Pharmacological Bulletin

摘　　要：目的研究延胡索乙素（dl-tetrahydropalmatine，dl-THP）对大鼠局灶性脑缺血再灌注损伤的保护作用。方法采用非开颅可逆性大鼠大脑中动脉栓塞法造成鼠脑缺血再灌注损伤。dl-THP10，20mg·kg-1在缺血前2min静脉注射。结果dl-THP可剂量依赖性缩小脑梗塞范围，减轻缺血再灌注脑电活动的抑制，明显减轻脑水肿，降低缺血再灌注引起的脑Ca2+聚集。结论dl-THP对大鼠局灶性脑缺血再灌注损伤具有保护作用，其机制可能与抑制脑组织Ca2+聚集有关。AIM To study the protective effects of dl-tetrahydrapalmatine (dl-THP) on focal brain ischemia-reperfusion injury in rats. METHODS Acute focal brain ischemia-reperfusion injury was produced by reversible middle artery occlusion without craniectomy in rats. dl-THP 5, 10, 20 mg· kg-1 was injected intravenously by 10 min before ischemia.RESULTS dl-THP dose-dependently decreased the size of cerebral infarction after ischemia for 2 h followed by reperfusion for 4 h. dl-THP also improved brain electrical activity, decreased the water content of injured brain, and reduced intracellular Ca2＋ accumulation resulted from ischemla-reperfusion event. CONCLUSION dl-THP had protective effects on acute focal brain ischemla-reperfusion injury. The drug might prevent the brain tissue from ischemia-reperfusion damage through reducing intracellular Ca2＋ accumulation resulted from ischemia-reperfusion event.

关 键 词：脑缺血 再灌注损伤 保护作用 延胡索乙素 

分 类 号：R743.310.5[医药卫生—神经病学与精神病学] R282.71[医药卫生—临床医学]