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机构地区:[1]东南大学附属中大医院神经内科
出 处:《卒中与神经疾病》2007年第6期330-333,共4页Stroke and Nervous Diseases
摘 要:目的观察脑慢性低灌注对老龄大鼠海马组织ε型蛋白激酶C(PKCε)及α分泌酶ADAM17蛋白表达的影响。方法将老龄大鼠随机分为假手术组和低灌注组,低灌注组永久性阻断双侧颈总动脉,制作脑慢性低灌注模型;采用Y型电迷宫分别于术后14和28d检测大鼠学习记忆能力;采用免疫组化法和免疫印迹法检测上述时间点海马组织PKCε和ADAM17的表达。结果低灌注组术后14和28d学习记忆能力较假手术组减退(P<0.01);与假手术组比较,低灌注组术后各时间点大鼠海马PKCε和ADAM17表达明显下降(P均<0.01)。结论脑慢性低灌注损害老龄大鼠学习记忆能力,导致痴呆发生,其机制可能与海马PKCε表达下降有关,而PKCε参与调节α分泌酶的表达,推测PKCε表达的下调,导致ADAM17表达减少,间接促进β淀粉样蛋白(Aβ)生成,损伤脑组织形成痴呆。Objective To explore the effect of chronic cerebral hypoperfusion on the expresstions of protein kinase C epsilon (PKCε) and tumor necrosis factor-alpha converting enzyme (TACE/ADAM17) in hippocampal of old rats. Methods Wistar rats were divided randomly into two groups: vascular occlusion (2VO) model group and sham-operated group. Permanent bilateral carotid artery occlusion (2VO) models were established to mimic the chronic cerebral hypoperfusion. Learning and memory abilities in rats were assessed by the Y-maze test at 14 and 28 days after operations. The expression of PKCε and ADAM17 protein were detected by immuno-histochemistry and western blotting at different times respectively. Results The learning and memory abilities of the rats declined at 14 and 28 days after 2VO (P〈0. 01). The expressions of PKCε and ADAM17 were lower in the 2VO model group than those in the shan-operated group. Conclusions The decreased expression of PKCε and ADAM17 in hippocampal may have participated in the occurrence of dementia after chronic cerebral hypoperfusion.
关 键 词:脑慢性低灌注 ε型蛋白激酶C α-分泌酶(ADAM17) 痴呆
分 类 号:R741[医药卫生—神经病学与精神病学]
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