黄芩素甙对脑缺血后大鼠海马组织兴奋性氨基酸含量的影响

Effects of Breviscarpin on Excitatory Amino Acid in Hippocampus of Rats Following Transient Cerebral Ischemia

目的观察黄芩素甙对脑缺血后大鼠海马组织兴奋性氨基酸含量的影响，探讨黄芩素甙脑保护作用的机制。方法42只雄性SD大鼠，体质量220～300g，随机分成3组：假手术组（Sham组，n=6）、对照组（Con组）和黄芩素甙组（Bre组）；后2组又分为再灌注6h、再灌注2d和再灌注4d3个亚组，每组6只。采用四血管阻断法制作大鼠脑缺血模型，脑缺血时间10min。光镜下观察海马CA1区神经元的存活情况，应用反相高效液相法测定海马组织中谷氨酸（Glu）和天冬氨酸（Asp）的含量。结果再灌注4d时，Sham组海马CA1区仅有少量神经元死亡，Con组海马CA1区大量神经元死亡，Bre组可见部分神经元死亡；再灌注6h时，Con组和Bre组的Glu和Asp含量明显高于Sham组（P〈0．01），Bre组的Glu和Asp含量明显低于Con组（P〈0．05），再灌注2d时，Con组和Bre组的Asp含量亦明显高于Sham组（P〈0．05或P〈0．01）。结论黄芩素甙可能通过抑制脑缺血后兴奋性氨基酸含量的增加而发挥其脑保护作用。

Objective To determine the effects of breviscarpin on the excitatory amino acid in hippocampal of rats following transient cerebral ischemia,and investigate the possible mechanism of its effects. Methods 42 male SD rats,weighting 220---300 g,were randomly divided into three groups：sham group（Sham group,n= 6）, control group （Con group） and breviscarpin group（Bre group）. According to the reperfusion time,the two latter groups were further divided into reperfusion 6 h,2 d and 4d subgroups（each subgroup,n=6）. The rat model of cerebral ischemia was induced by occlusion the four-vessel for ten minutes. The sharp of surviving neurons in hippocampal CA1 region was observed in optical microscope. The levels of glutamate（Glu） and aspartic acid （Asp） were measured by high-performance liquid chromatography. Results After repefusion 4 days,only a small number of neurons died in hippocampal CA1 region in Sham group, a large number of neurons died in Con group, and Bre group showed that some neurons died; The contents of Glu and Asp of Con/Bre groups were both significantly higher than that of sham group after reperfusion 6 hours（P〈0.01）. The levels of Glu and Asp of Bre group were significantly lower than that of Control group after reperfusion 6 hours（P〈0.05）. After repefusion 2 days,the contents of Asp of Con/Bre groups were both significantly higher than that of sham group（P〈 0.05 or P〈0.01）. Conclusion Breviscarpin can decrease the contents of of Glu and Asp after cetebal ischemia. And it may be the mechanism on the neuroprotective effect of breviscapin.