检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:张戈[1] 章翔[2] 费舟[2] 李兵[2] 梁景文[2]
机构地区:[1]广州军区武汉总医院神经外科,430070 [2]武汉第四军医大学西京医院全军神经外科研究所
出 处:《卒中与神经疾病》2003年第2期71-74,共4页Stroke and Nervous Diseases
摘 要:目的 研究大鼠全脑缺血再灌注损伤后酪氨酸羟化酶 (TH)和多巴胺 β 羟化酶 (DβH)表达的改变及意义。方法 利用改良四血管闭塞法 ,建立大鼠全脑缺血模型。于缺血再灌注后 1,3,5d断头取脑 ,行免疫组化染色 ,在光镜下观察海马CA1区神经元TH及DβH表达的变化 ,并计数海马CA1区正常神经元。结果 全脑缺血再灌注后 1d ,TH及DβH的表达呈阴性 ,海马CA1区神经元未见显著的病理形态学改变 ;全脑缺血再灌注后 3d ,TH及DβH呈阳性表达 ,海马CA1区可见部分神经元死亡 ;全脑缺血再灌注后 5d ,TH及DβH呈明显阳性表达 ,海马CA1区可见大部分神经元死亡。结论 全脑缺血再灌注后 ,由于TH及DβH异常表达 ,使得儿茶酚胺生物合成增加 ,这可能是短暂性脑缺血损伤的机理之一。Objective To study the changes and roles of tyrosine hydroxylase and dopamine-β-hydroxylase in rat hippocampal CA 1 region after cerebral ischemic-reperfusion injury. Methods Four-vessel occlusion was used to establish the globe brain ischemia model in rats. The rats were decapitated at 1, 3, 5 days after ischemia respectively. TH and DβH in hippocampus CA 1 region were detected by immunohistochemistry method and the alterations were observed under the light microscope. The number of normal neurons in the same region was also counted under the light microscope. Results No TH and DβH positive neuron was detected in hippocampus CA 1 region 1 d post-ischemia, and the change of pathomorphology was not detected either. In 3 d post-ischemic group, the TH and DβH positive neurons were detected in hippocampus CA 1 region, and part of the hippocampus CA 1 region neurons were dead. In 5 d post-ischemic group, the TH and DβH positive neurons were also detected in hippocampus CA 1 region, and nearly all of the neurons in this region were found dead. Conclusions Abnormal expression of TH and DβH after cerebral ischemic injury can raise the density of catecholamine in the brain, which could be one of the mechanisms that cause transient cerebral ischemia injury.
关 键 词:脑缺血 再灌注损伤 海马CAL区 神经元 酪氨酸羟化酶 多巴胺-Β-羟化酶
分 类 号:R743.31[医药卫生—神经病学与精神病学]
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.198