文献类型：期刊文献

中文题名：当归挥发油对化学性缺氧小鼠脑损伤的保护作用研究

英文题名：Study of Angelica naphtha on the protective action of cerebral injury of mice with chemical hypoxia

作者：罗慧英[1];杨焕[1];刘渊[1];李思[1];邱瑞玉[1]

第一作者：罗慧英

机构：[1]甘肃中医学院药理教研室

第一机构：甘肃中医药大学药学院（西北中藏药协同创新中心办公室）

年份：2011

卷号：28

期号：6

起止页码：5

中文期刊名：甘肃中医学院学报

外文期刊名：Journal of Gansu College of Traditional Chinese Medicine

基金：兰州市科技局科研项目(2010-1-213)

语种：中文

中文关键词：当归挥发油;化学性缺氧;脑损伤;能量代谢;兴奋性氨基酸

外文关键词：Angelica naphtha; chemical hypoxia; cerebral injury; energy metabolism; excitatory amino acid

摘要：目的初步探讨当归挥发油对化学性缺氧小鼠脑损伤的保护作用。方法将40只昆明种小鼠随机分为4组(空白组、模型组及当归挥发油高、低剂量组),灌胃给药7 d后,于最后1次给药2 h后腹腔注射亚硝酸钠800 mg/kg,记录各组小鼠的存活时间,检测脑组织中Na+-K+-ATPase,Ca2+-Mg2+-ATPase活性和乳酸(LD)含量,并测定脑组织中兴奋性氨基酸(EAA)谷氨酸(Glu)、天冬氨酸(Gly)、γ-氨基丁酸(GA-BA)及甘氨酸(Asp)的含量。结果当归挥发油可显著延长化学性缺氧小鼠的存活时间,增强Na+-K+-AT-Pase及Ca2+-Mg2+-ATPase活性,降低LD,Glu,GABA以及Gly含量,且作用呈剂量依赖性,对Asp无明显影响。结论当归挥发油能明显降低缺氧小鼠脑组织中EAA含量,并改善能量代谢,从而发挥对化学性缺氧脑损伤的保护作用。
Objective To study the protective action of Angelica naphtha on cerebral injury of mice with chemical hypoxia.Methods 40 mice were randomly divided into 4 groups： blank group,model group,high and low dose group of Angelica naphtha.After administrated with drug for 7 days,the cerebral injury model of chemical hypoxia was made by injecting NaNO2（800 mg/kg） in abdominal cavity of mice,and then wrote down the existent time of mice,detected the activity of Na＋-K＋-ATPase and Ca2＋-Mg2＋-ATPase,and the contents of lactic acid（LD）,glutamate（Glu）,glycine（Gly）,gama-aminobutyric acid（GABA） and aspirate（Asp） in brain tissue.Results Angelica naphtha could significantly lengthen the existent time of chemical hypoxia mice,increase the activity of Na＋-K＋-ATPase and Ca2＋-Mg2＋-ATPase,decrease the contents of LD,Glu,GABA and Gly in brain tissue,and the effects had dose dependent.Angelica naphtha hadn＇t obviously effect on Asp.Conclusion Angelica naphtha can obviously reduce the content of excitatory amino acid（EAA） in brain tissue of hypoxia mice,and can improve energy metabolism,thus develop the protective effect on cerebral injury of chemical hypoxia.