桂利嗪对兴奋毒损伤的海马神经元保护作用及其机制的实验研究  

Experimental Studies on Protective Effects of Cinnarizine on Neurons Injuried by Excitotoxicity

作　　者：王羽[1] 董志[2] 朱丽霞[2] 苏援淇[2] 廖红[2] 

机构地区：[1]重庆医科大学附属第二医院,重庆400010 [2]重庆医科大学药理教研室,重庆400016

出　　处：《中国药学杂志》2006年第20期1549-1552,共4页Chinese Pharmaceutical Journal

摘　　要：目的研究桂利嗪(Cin)对兴奋毒喹啉酸(QA)损伤的海马神经元是否有保护作用,并研究其相关机制。方法采用海马神经元原代培养,检测培养神经元的存活率、乳酸脱氧酶(LDH)活性,并观察其病理形态学改变,利用海马神经元损伤细胞模型,通过检测各组神经元的丙二醛(MDA)含量、一氧化氮合酶(NOS)活性及细胞内游离Ca2+浓度来探讨Cin对QA损伤海马神经元保护作用及其相关作用因素。结果Cin可提高QA损伤的原代培养海马神经元的脑细胞存活率,减少神经元LDH释放,并能减轻神经元的病理形态学损伤,可降低QA损伤海马神经元的MDA含量、NOS活性及胞内游离Ca2+浓度。结论Cin对QA所致的海马神经元损伤有明显的保护作用,其保护作用可能与下列因素有关:①降低细胞内Ca2+浓度;②减少自由基生成,促进自由基的清除;③降低NOS的活性,减少NO的生成。OBJECTIVE To study the protective effect of Cin on the hippocampus neurons injuried by quinolinic acid in vitro and its probable mechanisms. METHODS Hippocampus neurons were primarily cultured by using embryo rat brains. The activity of LDH of the cultured neurous were assayed and their pathological changes were also observed. Furthermore, the hippocampus neurous damaged by quinolinic acid, the content of MDA, the activity of NOS, the concentration of free Ca^2＋ were assayed and the apoptosis was observed. The protection of Cin on neurons injuried by quinolinic acid（QA）and the corresponding protective factors were estimated.RESULTS Cin increased the survival rate of hippocaznpus neurons in vitro damaged by QA. It diminished the release of LDH and improved the pathological morphology, and also decreased the content of MDA, the activity of NOS and the concentration of free Ca^2＋ . CONCLUSION Cin can protect the hippocampus neurons from quinolinic acid damage in vitro, and its probable mechanims were as follows： ①The concentration of free Ca^2 ＋ is decreased; ②The producing of free base is inhibited and the cleanance of free base is promoted; ③The activity of NOS is inhibited and the producing of NO is decreased.

关 键 词：海马神经元 兴奋毒 桂利嗪 喹啉酸 

分 类 号：R965[医药卫生—药理学]