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机构地区:[1]泉州市第一医院神经内科,福建省泉州市362000 [2]沈阳铁路局中心医院神经内科,辽宁省沈阳市110005
出 处:《中国临床康复》2003年第16期2315-2316,共2页Chinese Journal of Clinical Rehabilitation
摘 要:目的观察胰岛素(insulin,RI)对缺血再灌注损伤后细胞凋亡及其相应基因的调控作用,评估RI对脑缺血再灌注损伤的保护作用。方法将健康wistar大鼠56只,随机分为对照组、缺血再灌注盐水组(NS)、缺血再灌注胰岛素组(RI)。采用pulsinelli4血管阻塞模型,观察RI、NS在4,24,48h海马CA1区存活神经元数目,TUNEL阳性细胞数目,Bcl-2蛋白的表达,以观察比较缺血再灌注阶段细胞凋亡的变化。结果再灌注NS组CA1区神经元数目(36±6)个/mm2较再灌注RI组(88±9)个/mm2少(t=3.34,P<0.01)。再灌注后CA1区细胞凋亡数:4h时再灌注NS组(12±3)个/mm2高于再灌注RI(8±1)个/mm2和假手术组(2±1)个/mm2:组间比较,F=127.66,P<0.001。Bcl-2对海马CA1细胞凋亡评估4h时,再灌注NS组43.0±9.8,高于再灌注RI组24.0±5.4和假手术组2.7±0.8。结论全脑缺血再灌注时急用RI可减轻脑缺血再灌注神经元凋亡,对脑缺血再灌注损伤引起的神经元延迟性坏死有保护作用。Aim To evaluate the effects of insulin(RI) on neuronal apoptosis after cerebral ischemia reperfution in the Wistar rats.Methods Pulsilli's methods were employed to establish bllod embolism model in Wistar rats.56 rats were randomly divided into three groups:insulin reperfusion group(RI),salt fluid reperfusion group(NS) and control group.The influnces of RI and NS on the neuronal apoptosis were observed by calculating the number of surviving neurons,TUNEL positive neuron, expression of Bcl 2 in CA1 area of hippcampus.Results The number of neuron in CA1 region was (36±6)/mm2 in ischemia reperfusion NS group and (88±9)/mm2 in ischemia reperfusion RI group,with a significant difference(t=3.34,P< 0.01).The number of apoptosis cell in CA1 region in NS group[(12±3)/mm2] was more than that in RI group[(8±1)/mm2] and in sham operation group[(2±1)/mm2] at 4 h after reperfusion(F=127.66,P< 0.01).Expression of Bcl 2 in CA1 region in NS group (43.0±9.8) was higher than that in RI group(24.0±5.4) and in sham operation(2.7±0.8) at 4 h post reperfusion respectively.Conclusion RI has a remarkable pretection on cerebral ischemia reperfusion damage.Its mechanism may be related with the decrease of the neuronal apoptosis.
关 键 词:胰岛素 大鼠 脑缺血 再灌注损伤 神经元细胞凋亡 基因调控
分 类 号:R743.31[医药卫生—神经病学与精神病学]
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