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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。
Objective To investigate the protective effect of ginkgolide K (GNK) on focal cerebral ischemia-reperfusion (MCAO) injury in rats. Methods The rat model of ischemia reperfusion induced by ginkgolide for 2 h was used to investigate the effects of ginkgolide K on the symptoms of neurological deficit, the percentage of cerebral infarction, the water content of brain tissue, the activity of superoxide dismutase (SOD) (MDA) content and [Ca2 +] i concentration in cortical neurons, Bax protein, Bcl-2 protein and caspase-3 protein. Results Compared with cerebral ischemia-reperfusion group, the neurological deficit score, brain water content and percentage of cerebral infarction in GNK (4 and 8 mg.kg-1) groups were significantly decreased (P <0.01) (P <0.01). The protein expressions of Bax and caspase-3 were significantly decreased, while the expression of Bcl-2 protein was significantly increased. Conclusion Ginkgolide K has a protective effect on focal cerebral ischemia-reperfusion injury in rats. This mechanism may be related to the fact that Ginkgolide K reduces the concentration of [Ca2 +] i in brain tissue, anti-free radical injury And its inhibition of Bax and Bcl-2 protein expression and caspase-3 protein expression.