傅里叶变换红外光谱分析NMDA受体单克隆抗体抗兴奋毒损伤机理  

Fourier Transform Infrared Spectroscopic Investigation of Excitotoxicity-protective Mechanism of Monoclonal Antibody Against NMDAR

作　　者：康晓楠[1] 孙长凯[1] 范明[2] 宋占军[3] 赵杰[1] 王吉庆[4] 施广霞[5] 

机构地区：[1]大连医科大学脑疾病研究所,大连116027 [2]军事医学科学院基础医学研究所,北京100850 [3]军事医学科学院国家生物医学分析中心,北京100850 [4]解放军第210医院,大连116021 [5]大连医科大学病理生理学教研室,大连116027

出　　处：《生物化学与生物物理进展》2003年第2期290-294,共5页Progress In Biochemistry and Biophysics

基　　金：国家自然科学基金资助项目 (3 0 0 70 2 67);中国博士后科学基金(2 0 0 1);辽宁省重点科技攻关课题项目(2 0 0 12 2 60 0 5 )~~

摘　　要：人N 甲基 D 门冬氨酸受体 (NMDAR ,NR)单克隆抗体MABN1具有明确的抗兴奋毒保护作用 ,但其机制不明 .以MABN1和MK 80 1分别预处理海马细胞 ,拮抗谷氨酸兴奋毒损伤作用 ,采用傅里叶变换红外光谱(FTIR)技术 ,对不同处理后的海马细胞红外光谱特性进行比较 .将去卷积的酰胺Ⅰ带进行曲线拟合后发现 ,MABN1组与MK 80 1组的蛋白质二级结构有明显不同 。The monoclonal antibody MABN1 against NMDAR could protect the neurons from excitotoxicity, but the mechanism is unknown. Cultured hippocampus neurons treated with glutamate or/and NMDAR antagonist (MABN1 and MK 801) were studied by FTIR spectroscopy. Spectroscopic differences were observed between MABN1 treated and MK 801 treated samples. Curve fitting of the deconvoluted amideⅠband revealed the difference of protein second structure between MABN1 protected neurons and glutamate treated neurons, by which it was presumed that MABN1 protects neurons against excitotoxicity by the mechanism different from the one of MK 801.

关 键 词：博里叶变换红外光谱分析 NMDA受体 单克隆抗体 兴奋毒损伤 机理 海马神经元 谷氨酸受体离子通道 中枢神经系统 

分 类 号：Q423[生物学—神经生物学]