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缺血后适应对大鼠局灶性脑缺血再灌注后谷氨酸的影响 被引量:3

Effect of ischemic postconditioning on glutamate levels after focal cerebral ischemia reperfusion in rat
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摘要 目的:研究缺血后适应对大鼠局灶性脑缺血再灌注后谷氨酸(Glu)浓度变化的影响。方法:建立大鼠大脑中动脉阻塞(middle cerebral artery occlusion,MCAO)模型,将36只雄性SD大鼠随机分为假手术(Sham)组、脑缺血再灌注(I/R)组和缺血后适应(I Postcond)组,每组12只。应用高效液相色谱检测缺血脑组织匀浆Glu浓度。结果:局灶脑缺血再灌注6 h后,I Postcond组Glu浓度相较I/R组明显降低(P<0.01),局灶脑缺血再灌注24 h后,I Postcond组Glu浓度较I/R组低,但两者差异亦无显著性(P>0.05)。结论:本研究表明,I Postcond能够减轻MCAO大鼠模型中I/R损伤。细胞间隙Glu清除的加速可能是其重要保护机制之一。 Objective: To investigate the effect of ischemic postconditioning on glutamate after focal cerebral ischemia reperfusion.Methods: The MCAO(middle cerebral artery occlusion) models of rats were made.36 male Sprague-Dawley rats were randomly divided into 3 groups(n=12): Sham-operate(Sham) group,ischemia/reperfusion(I/R) group and ischemic postconditioning(I Postcond) group.We used high performance liquid chromatography(HPLC) to examine the glutamate concentration of the ischemic brain tissue homogenate.Results:The extracellular concentrations of glutamate were significantly lower in the I Postcond group compared with the I/R group(P〈0.01) 6 hours after reperfusion.The extracellular concentrations of glutamate were lower in the I Postcond group compared with the I/R group 24 hours after reperfusion,but no significant differences between them(P〉0.05).Conclusion: The present study showed that I Postcond alleviates I/R injury in MCAO rat model.Accelerating the elimination of glutamate in extracellular space might play an important role on this effect.
出处 《神经解剖学杂志》 CAS CSCD 北大核心 2011年第6期628-632,共5页 Chinese Journal of Neuroanatomy
基金 武汉市科技计划项目(20066009138-09)
关键词 缺血后适应 缺血再灌注 谷氨酸 大脑中动脉阻塞 大鼠 ischemic postconditioning ischemia/reperfusion glutamate middle cerebral artery occlusion rat
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  • 1Goldstein LB, Bushnell CD, Adams R J, Appel U, Braun LT, Chaturvedi S, et al. Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association/ American Stroke Association. Stroke 2011; 42: 517-84.
  • 2Carandang R, Seshadri S, Beiser A, Kelly-Hayes M, Kase CS, Kannel WB, et al. Trends in incidence, lifetime risk, severity, and 30-day mortality of stroke over the past 50 years. JAMA 2006; 296: 2939- 46.
  • 3Davis SM, Lees KR, AIbers GW, Diener HC, Markabi S, Karlsson G, et al. Selfotel in acute ischemic stroke: possible neurotoxic effects of an NMDA antagonist. Stroke 2000; 31: 347-54.
  • 4Sun HS, Jackson MF, Martin LJ, Jansen K, Teves L, Cui H, et al. Suppression of hippocampal TRPM7 protein prevents delayed neuronal death in brain ischemia. Nat Neurosci 2009; 12: 1300-7.
  • 5Lipton P. Ischemic celt death in brain neurons. Physiol Rev 1999; 79: 1431-568.
  • 6Sattler R, Tymianski M. Molecular mechanisms of calcium-dependent excitotoxicity. J Mol Med 2000; 78: 3-13.
  • 7Macdonald J, Xiong Z, Jackson M. Paradox of Ca^2+ signaling, cell death and stroke. Trends Neurosci 2006; 29: 75-81.
  • 8Choi DW. Glutamate neurotoxicityand diseases of the nervous system. Neuron 1988; 1: 623-34.
  • 9Horn J, Limburg M. Calcium antagonists for acute ischemic stroke. Cochrane Database Syst Rev 2000; (2): CD001928.
  • 10Tymianski M, Charlton MP, Carlen PL, Tator CH. Secondary Ca^2+ overload indicates early neuronal injury which precedes staining with viability indicators. Brain Res 1993; 607: 319-23.

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