延胡索乙素抗脂质过氧化作用与对脑缺血再灌注大鼠行为及病理改变的保护  

Antilipid peroxidation and protective effects of dltetrahydropalmatine on ischemia reperfusion neurological damage and abnormal behavior in rats

作　　者：梁健[1] 王富强[1] 郑平香[1] 梁京生 

机构地区：[1]广州医学院药理学教研室

出　　处：《中国药理学通报》1999年第2期167-169,共3页Chinese Pharmacological Bulletin

摘　　要：目的研究延胡索乙素（ｄｌｔｅｔｒａｈｙｄｒｏｐａｔｍａｔｉｎｅ，ｄｌＴＨＰ）抗脂质过氧化作用与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拴塞法造成大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可显著减轻神经功能障碍及脑组织病理损害，阻止脑组织超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ，ＳＯＤ）及乳酸脱氢酶（ｌａｃｔｉｃｄｅｈｙｄｒｏｇｅｎａｓｅ，ＬＤＨ）活力下降，阻止外周血中ＬＤＨ活力增加并阻止脑组织脂质过氧化产物丙二醛（ｍａｌｏｎｄｉａｌｄｅｈｙｄｅ，ＭＤＡ）含量增加。结论ｄｌＴＨＰ对大鼠局灶性脑缺血再灌注损伤有保护作用，机制可能与抗脂质过氧化反应有关。AIM To study the protective effects of dltetrahydrapalmatine (dlTHP) on focal brain ischemiareperfusion injury in rats. METHODS Acute focal brain ischemiareperfusion injury was produced by reversible middle artery occlusion without craniectomy in rats. dlTHP 10, 20 mgkg-1was injected intravenously by 2 min before ischemia. RESULTS dlTHP dosedependently reduced the score of neurological deficits and the ischemiareperfusion injury of brain tissue. dlTHP suppressed the reduction of superoxide dismutase (SOD) activities and lactic dehydrogenase (LDH) activities in brain tissue, decreased the content of malondiadehyde (MDA) in brain. dlTHP also decreased the rise of LDH activities in blood. These results indicate that dlTHP has protective effects against cerebral ischemia reperfusion injury probably through inhibiting free radical and subsequent lipid peroxidation.

关 键 词：脑缺血 再灌注损伤 延胡索乙素 抗氧化作用 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R977.9[医药卫生—临床医学]