中文摘要：

目的探讨银杏叶内酯K（ginkgolide K,GNK）对大脑局灶性脑缺血再灌注（MCAO）损伤大鼠的保护作用。方法采用栓线法大鼠缺血2 h再灌注22 h模型,探讨银杏内酯K对模型大鼠神经缺损症状、脑梗死百分比、脑组织含水率、超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量及皮层神经元细胞内[Ca2＋]i浓度、Bax蛋白,Bcl-2蛋白及caspase-3蛋白的影响。结果与脑缺血再灌注组相比,GNK（4和8 mg.kg-1）组中大鼠神经缺损评分、脑含水率、脑梗死百分比显著降低（P〈0.01）;脑组织丙二醛含量减少、SOD活性升高、[Ca2＋]i显著下降（P〈0.01）,Bax和caspase-3蛋白表达显著降低,Bcl-2蛋白表达显著提高。结论银杏内酯K对局灶性脑缺血再灌注损伤大鼠具有保护作用,本作用机制可能与银杏内酯K减少大鼠脑缺血再灌注后脑组织[Ca2＋]i浓度、抗自由基损伤及其抑制Bax与Bcl-2蛋白表达比例及caspase-3蛋白表达有关。

英文摘要：

OBJECTIVE To investigate the protective effect of ginkgolide K on cerebral focal ischemia reperfusion injury induced by middle cerebral artery occlusion（MCAO）in rats.METHODS The rat model of ischemia（2 h）and reperfusion（22 h）induced by thread approach were established for observing the effect of ginkgolide K on the neurological deficit score,infarction areas percentage,brain water content.In addition,malondialdehyde（MDA）and superoxide dismutase（SOD）,as well as intracellular Ca2＋iconcentration,Bax protein,Bcl-2 protein and caspase-3 protein in the cerebral cortex after 24 h of MCAO in rats were determined to investigate the anti-oxidative action and anti-neurotoxicity property of ginkgolide K.RESULTS Compared with MCAO group,GNK（4,8 mg·kg-1） group relieved obviously the neurological dificit score and reduced the cerebral infarction areas percentage,brain water content,intracellular Ca2＋iconcentration and MDA,Bax protein expression,and caspase-3 protein expression.Moreover,GNK（4,8 mg·kg-1）group improved the SOD activity and Bcl-2 protein expression after 24 h of MCAO in rats.CONCLUSION Ginkgolide K has protective effect on MCAO injury in rats,which may be related to reduce intracellular Ca2＋i concentration content,Bax/Bcl-2 protein expression ratio and caspase-3 protein expression and increase the antioxidant capacity.