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目的:探讨银杏叶内酯N(ginkgolide N,GN)对实验性大鼠大脑局灶性脑缺血再灌注损伤的保护作用。方法:采用栓线法阻断大鼠大脑中动脉缺血2 h后再灌注22 h模型,探讨银杏内酯N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)含量及大脑皮层神经元细胞内[Ca2+]i水平影响。结果:与假手术组相比,缺血再灌注组神经缺损评分、含水率、梗死率、脑组织MDA含量增加、SOD活性降低及[Ca2+]i显著升高(P<0.01);与脑缺血再灌注组相比,GN高、中、低剂量组,阳性对照组脑组织MDA含量减少、SOD活性升高、[Ca2+]i显著下降(P<0.01或P<0.05),GN高、中剂量组,阳性对照组大鼠神经缺损评分、脑含水率、脑梗死率显著降低(P<0.01);GN各剂量组间结果亦有显著差异(P<0.01或P<0.05)。结论:GN对局灶性脑缺血再灌注损伤大鼠具有保护作用,可能与其减少大鼠脑缺血再灌注后脑组织[Ca2+]i浓度、抗自由基损伤有关。
Objective: To investigate the protective effect of ginkgolide N (GN) on focal cerebral ischemia-reperfusion injury in rats. Methods: The model of neurological deficit, the percentage of cerebral infarction, the percentage of cerebral infarction, the water content of superoxide dismutase (SOD) activity, malondialdehyde (MDA) content and [Ca2 +] i level in neurons of cerebral cortex. Results: Compared with the sham operation group, the neurological deficit score, water cut, infarct rate, MDA content in brain tissue increased, SOD activity decreased and [Ca2 +] i increased significantly (P <0.01) Compared with the blood reperfusion group, the levels of MDA and the activities of SOD in the high, middle and low doses of GN group and the positive control group were significantly decreased (P <0.01 or P <0.05) The neurological deficit score, brain water content and cerebral infarction rate were significantly decreased in the dose group and the positive control group (P <0.01). There was also significant difference between the various dose groups of GN (P <0.01 or P <0.05). CONCLUSION: GN has a protective effect on focal cerebral ischemia-reperfusion injury in rats, which may be related to the decrease of [Ca2 +] i concentration and anti-free radical injury after cerebral ischemia-reperfusion in rats.