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CJAP ›› 2016, Vol. 32 ›› Issue (2): 158-162.doi: 10.13459/j.cnki.cjap.2016.02.016

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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:

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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