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雷公藤内酯醇对大鼠脑局灶性缺血再灌注脂质过氧化损伤影响的实验研究
引用本文:韦登明,黄光照,张益鹄,饶广勋. 雷公藤内酯醇对大鼠脑局灶性缺血再灌注脂质过氧化损伤影响的实验研究[J]. 中国药学杂志, 2004, 39(4): 267-270
作者姓名:韦登明  黄光照  张益鹄  饶广勋
作者单位:1. 宁波大学医学院,浙江,宁波,315211
2. 华中科技大学同济医学院,湖北,武汉,430030
摘    要:
 目的 观察雷公藤内酯醇(TL)对大鼠脑局灶性缺血再灌注脂质过氧化损伤影响。方法 预防性给予TL(0.2,0.4mg·kg-1,腹腔注射)3 d,实验第4天制备大鼠局灶性脑缺血再灌注模型后仍同法腹腔注射TL。观察大鼠脑功能的变化及大脑中动脉闭塞侧脑皮质超微结构变化;检测大脑中动脉闭塞侧脑组织超氧化物歧化酶(SOD)、脂质过氧化物丙二醛(MDA)水平。结果 与损伤模型组比较,治疗组大鼠脑功能受损程度、大脑中动脉闭塞侧脑皮质电镜下神经细胞变性、坏死损伤程度明显改善;脑组织SOD水平显著升高、MDA水平显著下降。结论 TL对大鼠缺血再灌注脂质过氧化脑损伤有一定的保护作用。其作用机制可能与TL抗氧化作用有关。

关 键 词:雷公藤内酯醇  脑缺血再灌注
文章编号:1001-2494(2004)04-0267-04
收稿时间:2003-05-30;

Study on the influence of triptolide on cerebral injury induced by lipid peroxidation after focal ischemic reperfusion in rats
WEI Deng-ming,HUANG Guang-zhao,ZHANG Yi-gu,RAO Guang-xun. Study on the influence of triptolide on cerebral injury induced by lipid peroxidation after focal ischemic reperfusion in rats[J]. Chinese Pharmaceutical Journal, 2004, 39(4): 267-270
Authors:WEI Deng-ming  HUANG Guang-zhao  ZHANG Yi-gu  RAO Guang-xun
Affiliation:1.Department of Pathology,Medical School,Ningbo University,Ningbo 315211,China;2.Department of Forensic Pathology,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China
Abstract:
OBJECTIVE To study the effect of triptolide (TL) on cerebral injury induced by lipid peroxidation after focal ischemia reper-fusion in rats. METHODS TL at dose 0.2 or 0.4 mg·kg-1 was intraperitoneally injected once a day for 4 d. The focal cerebral ischemia reperfusion model was established with thread embolism of middle cerebral artery before TL injection on fourth day. Neurological deficit score was evaluated, the pathologic change of brain tissue was observed with electron microscope. The levels of SOD and MDA in cerebral tissue were measured. RESULTS Compared with the ischemia reperfusion group, the cerebral function of the rats in two TL-treated groups was markedly improved. The degree of neuronal degeneration and necrosis in cerebral tissue detected under electron microscope was significandy attenuated. The level of MDA in cerebral tissue was remarkably reduced, and the activities of SOD in cerebral tissue was significantly elevated. CONCLUSION The results suggested that TL had a potent neuroprotective effect on cerebral ischemia and reperfusion in rats. The mechanism may relate to the anti-peroxidation effect of TL.
Keywords:triptolide  ischemia reperfusion model  lipid peroxidation
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