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作 者:姜涛[1] 罗一峰[1] 张爱武[2] 徐如祥[3]
机构地区:[1]南方医科大学第三附属医院神经内科,广东广州510630 [2]中山大学附属第一医院神经科,广东广州510080 [3]北京军区总医院附属八一脑科医院,北京100700
出 处:《广州医学院学报》2014年第3期5-8,共4页Academic Journal of Guangzhou Medical College
摘 要:目的:探讨parulexin 1通道在缺血缺氧损伤中对神经元树突棘的作用。方法:体外培养SD大鼠海马神经元,实验分为3组:对照组、缺血缺氧组和pannexin 1阻断剂CBX预处理组。在干预24 h后对培养神经元进行DiI染色,图像分析树突棘长度和密度。结果:对照组:树突棘以蘑菇状或纤足形态出现;缺血缺氧组:树突棘主要类型是纤足。而缺少蘑菇状;CBX预处理组树突棘以蘑菇状为主。与对照组相比。缺血缺氧组的树突棘密度与树突棘长度均有所降低(P<0.001);与缺血缺氧组相比,CBX预处理组的树突棘密度有所增加(P<0.001),但树突棘长度更短(P<0.001)。结论:pannexin 1通道增加树突棘缺血缺氧损伤,应用pannexin 1通道阻断剂对树突棘起到保护作用,同时促进树突棘的再生。Objective:To explore the effect of pannexin 1 channel on neural dendritic spine after hypoxia-ischemia. Methods:The primary cultured hippocampal neurons were divided into control group, hypoxia-ischemia group and CBX pretreatment group. Twenty-four hours after OGD, DiI staining was performed on the cultured hippocampal neurons in each group, and the the density and length of the dendritic spines were measured with image analysis system. Results:The shape of the dendritic spines in the control group was thin or “mushroom-like.” The density of the dendritic spines was obviously reduced in the hypoxia-ischemia group, and most spines were thin; mushroom-like spines were lacking.In the CBX pretreatment group, the density of the dendritic spines was increased compared to that in the hypoxia-ischemia group, and the majority of spines were stubby.Compared with the control group, the spine density and spine length were significantly decreased in the OGD group (P〈0. 0001).Compared with the OGD group, the spine density was significantly increased, and spine length was significantly decreased in the CBX group (P〈 0.0001). Conclusion:Pannexin 1 channel aggravated ischemic hypoxia injury of the dendritic spine after hypoxia-ischemia, and the blocker CBX could protect the dendritic spine from it, and also could promote the regeneration of the dendritic spines.
关 键 词:pannexin1通道 缺血缺氧 树突棘
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