铜负荷大鼠基底节对肝豆灵代谢响应的~1H NMR研究

采用核磁共振氢谱(1H NMR)技术与多元统计分析相结合的方法,对肝豆灵对大鼠基底节铜损伤的调节机制进行研究。24只雄性Wistar大鼠随机分为正常组、模型组和肝豆灵组,每组8只,以铜负荷法造模。从造模第7周开始,肝豆灵组大鼠以肝豆灵灌胃。数据分析显示:与正常组比较,模型组的基底节细胞凋亡指数显著增高(p0.01);基底节组织中的谷氨酰胺、尿苷、苏氨酸含量升高(p0.05),甘露醇、腺苷、N-乙酰天冬氨酸、谷氨酸、N-乙酰谷氨酸(NAG)、天冬酰胺、乙酸、天冬氨酸、肌醇、三磷酸腺苷(ATP)含量降低(p0.05);与模型组相比,肝豆灵组的基底节细胞凋亡指数显著降低(p0.01);基底节组织中的谷氨酰胺、尿苷、乙酸、天冬氨酸含量降低(p0.05),甘露醇、腺苷、苏氨酸、N-乙酰天冬氨酸、谷氨酸、N-乙酰谷氨酸、天冬酰胺、肌醇、ATP含量升高(p0.05)。研究结果表明,肝豆灵可影响铜负荷大鼠基底节的代谢,对铜损伤具有一定的修复作用,其机制可能是通过调节氨的解毒和兴奋性氨基酸类神经递质的代谢,干预能量代谢,恢复神经元和神经胶质细胞功能。

Metabolic Response of Basal Ganglia in Copper-laden Rat to Gandouling Based on 1H NMR Spectroscopy

1H NMR spectroscopy combined with multivariate statistical method was introduced in this paper to explore the regulation effect of Gandouling on basal ganglia injury in copper-laden rats.24 male Wistar rats were randomly divided into control group,model group and Gandouling group,with 8 rats in each group.The rat model was established by copper-laden method.From the 7th week of modeling,Gandouling group was given Gandouling formula via gavage.Compared with the control group,the index of apoptosis cells in basal ganglia of model group increased significantly(p<0.01),and glutamine,uridine and threonine in basal ganglia were increased(p<0.05) while mannitol,adenosine,N-acetylaspartate,glutamate, N-acetylglutamine asparagine, acetate, aspartate,myo-inositol and ATP were decreased(p<0.05).Compared with the model group,the index of apoptosis cells in basal ganglia of Gandouling group was significantly decreased(p<0.01),and glutamine,uridine,acetate and aspartate were reduced(p<0.05) while mannitol,adenosine,threonine,N-acetylaspartate,glutamate, N-acetylglutamine, asparagine,myo-inositol and ATP were elevated(p<0.05).The results showed that Gandouling could influence the metabolism of basal ganglia in copper-laden rats,which has a certain therapeutic effect on damage caused by copper.The mechanism may be restoration of the functions of neurons and glial cells,through adjusting the detoxification of ammonia and metabolism of excitatory amino acid neurotransmitter and interfering the energy metabolism.