银杏叶提取物对小鼠脑缺血再灌注损伤的拮抗作用

目的　研究银杏叶提取物 (EGb76 1)对小鼠脑缺血再灌注损伤的拮抗作用及其作用机理。方法双侧颈总动脉加迷走神经结扎法 (左侧不完全结扎 )造成小鼠局部脑缺血 5min ,再灌注 30min。DTNB法测定谷胱甘肽过氧化物酶 (GSH px)活性 ;荧光分光光度法测定脑组织线粒体膜蛋白结合铽 ;被动性回避行为学模型检测小鼠记忆能力 ;海马形态学观察。结果　小鼠局部脑缺血再灌注后 ,海马GSH px活性降低 ,海马 ,下丘脑和皮质线粒体膜蛋白结合铽降低 ,说明结合钙升高 ,海马CA1区神经元损伤 ,小鼠的记忆能力下降。EGb76 1(2 5 ,5 0 ,10 0mg·kg- 1·d- 1,ig ,连续 7d)能逆转上述变化。结论　EGb76 1拮抗小鼠脑缺血再灌注损伤的作用与抗氧化及阻止线粒体膜蛋白结合钙增加有关

Protective effects of extract from leaves of Ginkgo biloba on focal cerebral ischemia-reperfusion injury in mice

AIM To investigate whether the extract from leaves of Ginkgo biloba(EGb761) can protect neurons from focal cerebral ischemia- reperfusion injury in mice. METHODS Focal cerebral ischemia(5 min) reperfusion(30 min) injury was induced by occlusion of common carotid artery and vagus nerve(the left was occluded incompletely). The activity of glutathione peroxidase(GSH-px) of hippocampus was determined by the method of DTNB. The mitochondrial membrane protein-bound Tb³⁺ fluorescent intensity was measured by fluorospectrophotometry. One-trial passive avoidance model was carried out for determining memory retention in mice. Morphological observation of hippocampus was made with a light microscopy. RESULTS ]After cerebral ischemia-reperfusion, GSH- px activity in hippocampus was decreased and mitochondrial membrane protein- bound Tb³⁺ fluorescent intensity in hippocampus, hypothalamus and cortex decreased, which indicated the increase in protein-bound Ca²⁺. Hippocampus CA1 neurons were damaged and memory retention was alleviated. However, the pretreatment with EGb761(25, 50, 100 mg·kg^-1·d^-1, ig for 7 d) reduced the above changes. CONCLUSION EGb761 Protects neurons from focal cerebral ischemia-reperfusion injury in mice by virtue of anti-oxidation and inhibition of Ca²⁺ overloading.