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作 者:李建民[1] 赵雅宁[2] 陈长香[2] 李淑杏[2] 王大永[3]
机构地区:[1]华北煤炭医学院附属医院神经外科,河北唐山063000 [2]华北煤炭医学院护理系 [3]河北省唐山工人医院神经外科
出 处:《中国公共卫生》2011年第2期208-209,共2页Chinese Journal of Public Health
基 金:河北省科技厅课题(09276103D-3)
摘 要:目的探讨川芎嗪预处理对沙鼠前脑缺血再灌注损伤的保护作用及机制。方法雄性沙鼠随机分为对照、脑缺血再灌注、缺血预处理、川芎嗪预处理组,参照Kirino法制备脑缺血再灌注模型,Kitagawa法制备脑缺血预处理模型,HE染色法观察海马区神经细胞形态变化,免疫组织化学法检测神经胶质纤维酸性蛋白(GFAP)表达,原位缺口末端标记法(TUNEL)检测神经细胞凋亡情况,4-pellet taking test(4-PTT)旱路迷宫法测试动物学习记忆功能。结果与脑缺血再灌注组比较,缺血预处理和川芎嗪预处理组中存活神经元密度(12.93±3.17,18.74±4.21)增加;GFAP(8.50±1.25,12.72±1.38)表达增加,凋亡神经细胞数量(16.50±5.25,9.72±3.38)下降;参照记忆指数和工作记忆指数得到改善(P均<0.05)。结论川芎嗪预处理可改善脑缺血再灌注沙鼠的学习记忆功能,其机制与增强星形胶质细胞活性、减少神经细胞凋亡有关。Objective To study the effect and possible protective mechanism of tetramethyl pyrazine(TMP) on cerebral ischemia/reperfusion injury in gerbils.Methods Male gerbils were divided randomly into four groups:control group,ischemia/reperfusion group(I/R),ischemia preconditioning group(IP),and TMP preconditioning group.Changes of neuron morphous in hippocampus region were observed by HE staining.The expression level of glial fibrillary acidic protein(GFAP) was detected with immunohistochemistry.Neuron apoptosis was detected with terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL) method.Learning-memory function was determined with 4-pellet taking test(4-PTT) dry path maze.Results Compared with I/R group,the density of survival neurons(12.93±3.17,18.74±4.21) and the expression levels of GFAP(8.50±1.25,12.72±1.38) were enhanced in IP group and TMP preconditioning group,and the apoptotic neurons(16.50±5.25,9.72±3.38) were decreased.Reference memory index and working memory index were improved(P0.05 for all).Conclusion TMP can improve learning-memory function in gerbils with cerebral ischemia/reperfusion damage and enhance ischemic tolerance,which might be associated with up-regulation of GFAP expression and down-regulation of neuron apoptosis.
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