连二亚硫酸钠致PC12和NG108-15细胞拟缺血损伤研究  

Researches on an ischemical model of PC12 and NG108 15 cell lines

作　　者：刘娜[1] 左萍萍[1] 周帆 张放 刘景生[1] 任民峰[1] 

机构地区：[1]中国医学科学院基础医学研究所中国协和医科大学基础医学院药理室

出　　处：《中国药理学通报》1998年第6期525-525,共1页Chinese Pharmacological Bulletin

摘　　要：目的利用稳定的细胞模型进行药物机制研究，对探讨药物等对缺血的影响十分重要。方法结合形态学和受体功能研究方法，利用连二亚硫酸钠消除培养基中的氧合并培养基质缺糖导致拟缺血细胞，并对其细胞功能和缺血机制进行了探讨。结果这种拟缺血模型造成了体外培养细胞上类似与体内细胞缺血的变化，细胞肿胀变性甚至坏死，细胞膜上兴奋性氨基酸（ＥＡＡ）的Ｎ甲基Ｄ天冬氨酸（ＮＭＤＡ）受体活性增强，伴随其他功能性受体如胆碱能（Ｍ、Ｎ）受体活性降低。经ＮＭＤＡ受体特异性拮抗剂———２氨基膦酸基戊酸（ＡＰＶ）作用后，ＮＭＤＡ受体激活明显被抑制，细胞所受缺血损伤也有减轻。同时将ＮＧ细胞与ＰＣ细胞的胆碱能受体活性变化进行了比较，发现ＮＧ活性变化与连二亚硫酸钠剂量变化关系更为稳定。结论提示利用连二亚硫酸钠可模拟体内缺血机制。AIM To establish a stable cellular model and obtain a relatively homogenous cell population for our studies of ischemia through a simple and effective episode. METHOD To investigate the molecular mechanism of neuronal ischemia, PC12 and NG108 15 cell lines were now popular in neuroscience research use. RESULT After 20 min exposed in a glucose free and hypoxia medium executed by Na 2S 2O 4(1,2,4 or 8 mmol·L -1 ), the MK801 binding or PC and NG cells was significantly higher than that in the control groups, while the binding activities of m , n cholinergic receptors in the same cells decreased as compared to the control. Morphologic changes also showed cells dysfunction. Futhermore, pretreatment of APV markedly lowered the NMDA receptor activities in the ischemic cells and the cells seemed better survival. CONCLUSION Ischemic model using Na 2S 2O 4 and glucose free medium may well build up the excessive activation of glutamate NMDA receptors and cholinergic dysfunction in cells.

关 键 词：连二亚硫酸钠 胆碱能受体 缺血损伤 

分 类 号：R971[医药卫生—药品] R364.12[医药卫生—药学]