摘要
目的 探讨诱导型一氧化氮合酶在血管性痴呆 (vasculardementia,VD)大鼠海马中的表达。方法 将 6 0只大鼠随机分为 5组 :对照组、模型 12h组 (VD12h)、模型 1d组 (VD1d)、模型 3d组(VD3d)、模型 7d组 (VD7d) ,每组 12只。采用反复夹闭双侧颈总动脉再灌注方法建立血管性痴呆大鼠模型。用HE染色观察各组大鼠海马CA1 区神经元数目的变化 ;应用免疫组织化学染色和WesternBlot方法检测诱导型一氧化氮合酶在大鼠海马中的表达。结果 大鼠海马CA1 区神经元数在 12h组、 1d组、 3d组、 7d组均明显下降。Western印迹显示在VD12h组iNOS的表达上调 ,VD1d组进一步升高 ,保持这一水平至第 7天。免疫组化见iNOS在正常组大鼠海马CA1区中有很弱的表达 ,在VD12h组、 1d组、 3d组、 7d组表达逐渐增强。结论 iNOS可能参与缺血后海马神经元的损害 ,是构成血管性痴呆的机制之一。
Objective To explore the expression of iNOS in the hippocampus in a rat model of vascular dementia.Methods The 60 rats were randomly divided into five groups:control group,12-hour model group,1-day model group,3-day model group,7-day model group, 12 rats in each group.Animal model of vascular dementia (VD) was established through repeated cerebral ischemia-reperfusion in rats.The number of neuron in CA 1 area of hippocampus in each group was observed with HE stain. Expression of iNOS in the hippocampus was measured with immunohistochemical staining and western blot methods. Results The number of neuron in CA 1 area of hippocampus decreased significantly in 12-hour group,1-day group,3-day group,and 7-day group.iNOS concentrations determined by western blot were up-regulated in 12-h group.The concentration increased further in 1-day group and maintained at this level to 7 day. Immunohistochemical staining showed that iNOS in CA 1 area of hippocampus had very weak expression in normal rats' group and increased gradually in 12-hour,1-day,3-day and 7-day group. Conclusions iNOS may be related to the injury of hippocampus neuronal cells in vascular dementia.It might be one of the reasons causing vascular dementia.
出处
《中华急诊医学杂志》
CAS
CSCD
2004年第9期606-608,i002,共4页
Chinese Journal of Emergency Medicine
