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作 者:张卫同[1] 柴栋[1] 徐珊[2] 刘萍[1] 刘坤[3]
机构地区:[1]解放军总医院海南分院药剂科,海南三亚570213 [2]海南医学院药学院,海口571199 [3]首都体育学院,北京100038
出 处:《中国应用生理学杂志》2014年第4期352-356,共5页Chinese Journal of Applied Physiology
基 金:国家自然科学基金面上项目(81173572)
摘 要:目的:研究脑缺血大鼠脑纹状体区细胞外液中氨基酸类神经递质的表达变化及对脑组织的保护作用;证明开窍药石菖蒲的有效成分对氨基酸类神经递质改变产生影响。方法:24只SD大鼠随机分为4组(n=6):正常对照组、脑缺血模型组、假手术组和药物组。用双侧颈动脉线栓法建立大鼠脑缺血模型后给予石菖蒲提取液,采用脑微透析技术在大鼠脑纹状体区域内进行活体采样,并联合使用高效液相色谱法检测样品中的谷氨酸、天门冬氨酸、甘氨酸、γ-氨基丁酸的含量。结果:与正常对照组相比,脑缺血期间4种氨基酸含量显著升高(P<0.01);与脑缺血模型组相比,石菖蒲给药组纹状体内天门冬氨酸、谷氨酸含量显著下降(P<0.01),甘氨酸、γ-氨基丁酸含量给药后2 h无显著性差异,以后甘氨酸、γ-氨基丁酸升高。结论:石菖蒲有效成分可降低因脑缺血而升高的谷氨酸、天门冬氨酸,因此减少兴奋性氨基酸过度释放的毒性,从而保护脑缺血后神经元的继发性损伤。Objective: To research the change of concentration of the amino acid in rat and the effect of Acorns tatarinowii Schott,one of inducing resuscitation drugs, for 4 of amino acid neurotransmitters. Meflmds: Twenty four rats were divided into four groups( n = 6) : control pup, cerebral ischemia group, sham operation group and Acorns tatarinowii Schott treated group. Rats were established into models of cerebral ischemia by occluding bilateral thread cork method. Formation sampling were performed in a striatum area using microdialysis and the detection of biological sample including aspartic acid, glutamic acid, glycine and γ- aminobutyric acid by high perfommnce liquid chromatography (HPLC) electrochemical detector system. Remits: Compared with the control, the all contents of 4 kinds of the amino acids were significantly increased during cerebral ischemia( P 〈 0.01). Compared with the cerebral ischemia group, the contents of aspartic acid, glutamic acid that were excitatory amino acids were remarkably decreased in the striatum for Acorns tatarinowii Schott treated group( P 〈 0.01), It was no significant influence on γ-aminobutyric acid and glycine that belonged to inhibitory amino acid in a nascent condition but with a elevating in the later period of microdialysis. Conclusion: Acorns tatarinowii Schott can enter the cerebral parenchyma through blood brain barrier and cut down glutamic acid, aspartic acid increased during cerebral ischemia. As a result, the neuroloxicity attributed to the excitatory amino acid has been released in excessive amounts declined so as to avoid the secondary impairment of neurons caused by excitatory amino acids pernicious effects after ischemia. It may be one of the protective mechanism of drugs for inducing resuscitation resembling EAA receptor antagonists to ischemi brain.
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