黄蜀葵总黄酮对全脑缺血损伤的保护作用  

Protective effect of abelmischl manihot l.medic against cerebral ischemia-reperfusion injury

作　　者：郭岩[1] 陈志武[1] 

机构地区：[1]安徽医科大学药理学教研室,合肥230032

出　　处：《中国药理学通报》2002年第6期692-695,共4页Chinese Pharmacological Bulletin

基　　金：安徽省自然科学基金资助课题 No 990 444 33

摘　　要：目的　研究黄蜀葵总黄酮 (TFA)对脑缺血及再灌注损伤的保护作用。方法　结扎双侧颈总动脉建立小鼠脑缺血模型 ,观察小鼠 6h存活率 ,测定缺血脑组织中丙二醛(MDA)含量 ;采用小鼠氮气缺氧模型 ,观察小鼠存活时间 ;采用结扎双侧颈总动脉合并血压下降法建立兔脑缺血再灌注模型 ,兔脑缺血 60min后再灌注 3 0min ,记录脑缺血和再灌注的脑电图 (EEG) ,测定缺血脑组织的丙二醛 (MDA)、乳酸脱氢酶 (LDH)。结果　TFA(3 0、60、12 0mg·kg-1)延长小鼠缺氧后的存活时间和提高脑缺血后小鼠的存活率及能抑制脑组织中MDA的增高。TFA(12、2 4、48mg·kg-1)抑制兔脑缺血再灌注损伤所致的EEG、MDA、LDH变化。结论　TFA对脑缺血及再灌注损伤有保护作用 。AIM To study the protective effect of TFA against cerebral ischemia reperfusion injury. METHORDS The cerebral ischemia model in mice was made by means of ligating bilalateral common carotid arteries.The mice survive rate during 6 h was observed,and malondialdehyde (MDA) in the ischemic cerebral cortex was measured. Using nitrogen anoxia model in mice,the survive time was observed. Ligating bilateral common carotid arteries and descending blood pressure,the cerebral ischemia reperfusion model in rabbits was established. The brain of rabbits was initiated by ischemia for 60 min followed by 30 min of reperfusion. The electroencephalogra phy (EEG) of cerebral ischemia and reperfusion was recorded. Malondialdehyde(MDA) and lactate dehydrogenase(LDH) in the ischemic cerebral cortex were measured. RESULTS TFA(30,60,120 mg·kg -1 ) prolonged the survive time after anoxia in mice,enchanced the survive rate after cerebral ischemia and inhibited the increasing of MDA contents in the cerebral cortex in mice.TFA(12,24,48 mg·kg -1 ) inhibitid the changes of EEG,MDA and LDH induced by cerebral ischemia reperfusion in rabbits. CONCLUSION TFA has protective effects on cerebral ischemia reperfusion injury,the mechanism may relate to attenuating free radical and lipid peroxidation.

关 键 词：黄蜀葵总黄酮 脑缺血 脑电图 丙二醛 乳酸脱氢酶 脑保护 黄蜀葵 

分 类 号：R277.733.1[医药卫生—中医学] R