摘要
目的研究尼莫通对大鼠急性脑缺血再灌注损伤后缺血半暗带神经元Na+-K+-ATP活性的影响。方法选取450只雄性Wistar大鼠随机分为3组(对照组、尼莫通组、假手术组),每组大鼠根据缺血后再灌注不同时间又分为缺血2 h再灌注6 h、24 h、48 h、72 h、7 d五个亚组(30只/亚组)。采用线栓法制备大鼠缺血2 h再灌注模型,仅尼莫通组采用药物进行干预。分别于再灌注6 h、24 h、48 h、72 h及7d断头取脑,观察缺血半暗带脑组织Na+-K+-ATP酶活性、脑组织水肿程度、脑梗死范围及神经症状评分的变化。结果三组间和不同时间点之间各项观察指标比较差异均有统计学意义(P<0.01);尼莫通组24 h、48 h、72 h各时间点Na+-K+-ATP酶活性及脑组织含水量与对照组相应时间点比较差异有统计学意义(P<0.05),尼莫通组24 h、48 h、72 h、7 d各时间点脑梗死面积及神经症状评分较对照组相应时间点显著降低,差异有统计学意义(P<0.05)。对照组大鼠脑缺血半暗带神经元Na+-K+-ATP酶活性于6 h开始降低,48 h达最低值,72 h稍有回升,7 d趋于稳定。结论尼莫通对大鼠急性脑缺血再灌注损伤后缺血半暗带神经元具有保护作用,其机制不仅与拮抗Ca2+超载有关,同时还可能与改善能量代谢有关。
Objective To study affection of nimotop on the Na＋-K＋-ATPase of neurons in ischemic penumbra in rats with acute cerebral ischemia-reperfusion injury.Methods Four hundred and fifty male Wistar rats were randomly divided into three groups（control group,nimotop group and sham operation group）;the 3 groups were further divided into 6 h,24 h,48 h,72 h and 7 d group according to the time of reperfusion.The rats model of ischemia reperfusion（2 h） were induced by thread approach.Only the nimotop group received medical interventions.The rats were executed at reperfusion 6 h,24 h,48 h,72 h,7 d to observe the neurological symptoms grade,the activities of Na＋-K＋-ATPase,the changes of brain water content and infarction size.Results The comparison of each observation index of the three groups and different time points reached statistical significance（P＆lt;0.01）.At 24 h,48 h and 72 h point,the activities of Na＋-K＋-ATPase and the brain water content in nimotop group were significant difference than in control group（P＆lt;0.05）.while,at 24 h,48 h,72 h and 7 d,the infarction size and neurological symptoms grade in nimotop group were significantly lower than control group（P＆lt;0.05）.The activities of Na＋-K＋-ATPase were down-regulated in control group,beginning at 6 h,bottoming at 48 h,up at 72 h and steadying at 7 d.Conclusion Nimotop have protective effect on neurons in ischemic penumbra in rats with acute cerebral ischemia-reperfusion injury,the mechanisms is related not only to the inhibition of calcium overload,but also to improving energy metabolism.
出处
《中国临床新医学》
2013年第3期195-199,共5页
CHINESE JOURNAL OF NEW CLINICAL MEDICINE
基金
广西自然科学基金资助项目(编号:桂科自0991212)
