依达拉奉对大鼠局灶性脑缺血的保护作用  

Neuroprotective effect of edaravone on focal cerebral ischemia in rats

作　　者：胡海涛[1] 吴继敏[1] 王爽[1] 

机构地区：[1]浙江大学医学院附属第二医院,浙江杭州310009

出　　处：《中国药学杂志》2005年第19期1463-1466,共4页Chinese Pharmaceutical Journal

摘　　要：目的探讨自由基清除剂依达拉奉对大鼠脑缺血及再灌注损伤的保护作用。方法大脑中动脉阻断法制备大鼠脑缺血再灌注模型,缺血60min后再灌注24h,术前30min及再灌注2h后尾静脉给药。观察不同浓度的依达拉奉对脑缺血再灌注引起的神经功能缺损症状及病理损伤的影响,检测脑组织内丙二醛(MDA)含量的变化以及脑组织超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)活性的变化。结果依达拉奉能轻度改善脑缺血再灌注24h后神经功能缺失症状;0.3～3.0mg·kg^(-1)依达拉奉能显著减少梗死体积和脑水肿,减少神经元损伤(P<0.05);依达拉奉剂量依赖性的降低脑组织MDA含量,增加LDH活性,0.3～3.0mg·kg^(-1)与对照组相比有显著性差异;但依达拉奉对脑组织SOD活性变化无明显影响。结论依达拉奉对大鼠脑缺血有保护作用,其机制可能与减轻脑水肿,清除自由基有关。OBJECTIVE To determine the neuroprotective effect of edaravone on focal cerebral ischemia in rats.METHODS Focal cerebral ischemia was induced by middle cerebral artery （MCA） occlusion for 60 min and followed by 24 h reperfusion. Edaravone （0.1 - 3.0 mg·kg^-1 ） or vehicle （ saline 2 mL·kg^-1） was injected intravenously 30 rain before MCA occlusion and after 2 h reperfusion. The neurological score, infarct volume, neuron density （in cortex, hippocampus, and striatum）, brain edema, malondialdehyde （MDA） content, superoxide dismutase （SOD） and lactate dehydrogenase （LDH） activity in brain tissue were determined after 24 h reperfusion.RESULTS Edaravone slightly improved the neurological deficiency, decreased infarct volume and neuron loss at the doses of 0.3, 1.0, 3.0 mg·kg^-1 （ p 〈 0.05）. The enlargement of the ischemic hemisphere was inhibited at the doses of 0.3, 1.0,3.0 mg·kg^-1. Edaravone markedly reduced MDA content and LDH activity at the doses of 0.3 - 3.0 mg·kg^-1. Edaravone had no effect on SOD activity. CONCLUSION Edaravone displays the protective effect on focal cerebral ischemia in rats, which is partially attributed to the inhibition of brain edema and the elimination of free radical.

关 键 词：依达拉奉 脑缺血再灌注 丙二醛 乳酸脱氢酶 超氧化物歧化酶 

分 类 号：R965[医药卫生—药理学]