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中国应用生理学杂志 ›› 2016, Vol. 32 ›› Issue (2): 158-162.doi: 10.13459/j.cnki.cjap.2016.02.016

• 研究论文 • 上一篇    下一篇

右美托咪定对脑缺血/再灌注大鼠海马兴奋性氨基酸含量及NMDA受体亚单位NR1表达的影响

尚宇1, 薛强1, 顾佩菲2, 李悦3, 高光洁1   

  1. 1. 解放军第四六三医院麻醉科, 辽宁 沈阳 110042;
    2. 东北制药集团市场部, 辽宁 沈阳 110016;
    3. 哈尔滨医科大学附属一院麻醉科, 黑龙江 哈尔滨 150001
  • 收稿日期:2015-09-06 修回日期:2016-01-25 出版日期:2016-03-28 发布日期:2018-06-12
  • 通讯作者: 高光洁,Tel:024-28845351;E-mail:guangjie420@126.com E-mail:guangjie420@126.com
  • 基金资助:
    辽宁省自然科学基金资助项目(2015020416)

Effect of dexmedetomidine on the changes of EAA and the expression of NMDA NR1 protein in hippocampus in global cerebral ischemia/reperfusion rats

SHANG Yu1, XUE Qiang1, GU Pei-fei2, Li Yue3, GAO Guang-jie1   

  1. 1. No. 463 Hospital of PLA, Shenyang 110042;
    2. Northeast Pharmaceutical Group, Shenyang 110016;
    3. The First-Affiliated Hospital of Harbin Medical University, Harbin 150001, China
  • Received:2015-09-06 Revised:2016-01-25 Online:2016-03-28 Published:2018-06-12
  • Supported by:
    辽宁省自然科学基金资助项目(2015020416)

摘要: 目的:观察右美托咪定预处理对全脑缺血/再灌注大鼠海马细胞外谷氨酸(Glu)、天门冬氨酸(Asp)含量及N-甲基-D-天冬氨酸(NMDA)受体1(NR1)表达的影响,探讨右美托咪定脑保护作用及其神经递质机制。方法:雄性Wistar大鼠54只,随机分为3组(n=18):假手术组、脑缺血/再灌注组和右美托咪定预处理组。用四血管闭塞法建立大鼠全脑缺血模型。收集清醒、缺血15 min及再灌注0~1 h微透析标本。于全脑缺血15 min再灌注1 h后,迅速断头取脑,采用免疫组化法和蛋白免疫印迹法检测海马NMDA受体NR1亚单位的表达情况。结果:与脑缺血/再灌注组相应时点比较,右美托咪定预处理组大鼠海马微透析液中Glu、Asp含量明显降低(P<0.05, 0.01);免疫组化和Western-blot法检测显示右美托咪定预处理组大鼠海马组织NMDA受体亚单位NR1表达明显受抑制(P<0.05, 0.01)。结论:右美托咪定预处理不仅减少脑缺血/再灌注时兴奋性氨基酸释放,还能抑制NMDA受体亚单位NR1的高表达而产生脑保护作用。

关键词: 右美托咪定, 缺血/再灌注损伤, 谷氨酸, 天门冬氨酸, NMDA受体, 大鼠

Abstract: Objective: To observe the effects of dexmedetomidine (DEX) on glutamate (Glu), aspartic acid (Asp) release and NMDAR1 expression in hippocampus in global cerebral ischemia/reperfusion rats, and investigate the protective effect and the related mechanism of neurotransmitters. Methods: Fifty-four male Wistar rats were randomly divided into three groups (n=18):sham group(A), ischemia/reperfusion group(B), dexmedetomidine pretreatment group(C). Total cerebral ischemia model was set up by four vessel occlusion in rats. Glu and Asp levels were measured with microdialysis at different time. Then the animals were decapitated and the brains were immediately removed to detect NMDAR1 expression in hippocampus area by immunohistochemistry and Western-blot. Results: Compared with that in group B, the levels of Glu, Asp and NMDA NR1 protein were significantly decreased in the dexmedetomidine pretreatment group (P<0.05 or 0.01). Conclusion: Dexmedetomidine might has a protective effect on hippocampus in global cerebral ischemia/reperfusion animals. The protective mechanism might be involved in inhibiting excitatory amino acids(EAA) release and NMDAR1 expression.

Key words: dexmedetomidine, ischemia/reperfusion injury, glutamate, aspartic acid, N-methyl-D-aspartate receptor, rat

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