摘要
目的:观察酸枣仁皂苷A对大鼠脑缺血海马区兴奋性氨基酸及细胞凋亡的影响,探讨酸枣仁皂苷A对脑缺血损伤保护的作用机制。方法:建立大鼠大脑中动脉闭塞再灌注损伤模型,将健康SD大鼠随机分为假手术组、缺血再灌注模型组、尼莫地平组、酸枣仁皂苷A组,四组于脑缺血再灌注后12、24、48小时、4天、7天,各取6只大鼠断头取脑,测定大鼠缺血侧脑海马区氨基酸递质水平及细胞凋亡数。结果:除假手术组外,与模型组比较,尼莫地平组和酸枣仁皂苷A组各观察时间点缺血侧脑海马区谷氨酸(Glu)及细胞凋亡均明显降低(P<0.05),而γ-氨基丁酸(GABA)在各时间点均明显升高;与尼莫地平组比较,酸枣仁皂苷A组大鼠缺血侧海马区Glu降低(P<0.05),酸枣仁皂苷A组细胞凋亡数降低更显著(P<0.05),两组GABA比较,差异无显著性意义(P>0.05)。结论:酸枣仁皂苷A能调节脑缺血损伤后海马区氨基酸水平的释放,抑制细胞凋亡。
Objective:To observe the effect of jujuboside A (JuA) on amino acids levels and apoptosis in hippocampus cerebral ischemia in rats and to probe into the neuro - protection mechanism of mild hypothermia on cerebral isehemie injury. Methods: Using the model of focal middle cerebral artery occluded, the healthy Wistar rats were randomly divided into sham group, cerebral isehemia model group, nimodipine group, and JuA treatment group. Every 6 rats in each group were sacrificed on 0.5d, 1d, 2d, 4d, and 7d after cerebral ischemia and reperfusion to determine amino acids and apoptosis levels in the brain. Results:Compared with the model group, the nimodipine and JuA groups had glutamic acid and apoptosis significantly decreased ( P 〈 0.05 ) and Gamma aminobutyric acid (GABA) increased at each time point except the Sham group. Compared with the nimodipine group, the level of glutamic acid and apoptosis reduced more significantly in the JuA group( P 〈 0.05 ), but the difference in GABA was not significant between the 2 groups( P 〉 0.05). Conclusion: JuA can regulate effectively the release of amino acid and decrease apoptosis in the hippocampus after cerebral iachemic injury.
出处
《浙江中西医结合杂志》
2009年第7期403-405,共3页
Zhejiang Journal of Integrated Traditional Chinese and Western Medicine
基金
广西壮族自治区科技厅资助项目(桂科基No.0575085)