N-甲基-D-天冬氨酸Ⅰ型受体在1，2-二氯乙烷急性中毒性脑病中的表达  

Expression of N-methyl-D-aspartate receptor-1 in acute intoxicated encephalopathy induced by 1,2- dichloroethane

作　　者：牛侨[1] 郭晓丽[1] 

机构地区：[1]山西医科大学公共卫生学院劳动卫生学教研室,太原030001

出　　处：《中华劳动卫生职业病杂志》2007年第2期65-68,共4页Chinese Journal of Industrial Hygiene and Occupational Diseases

基　　金：国家自然科学基金项目（30271116）

摘　　要：目的研究N-甲基-D-天冬氨酸Ⅰ型受体（NMDAR1）在1，2-二氯乙烷（1，2-DCE）急性中毒性脑病发病中的作用。方法SD大鼠42只，随机分为1个对照组、3个染毒组和3个染毒后时间观察组，每组6只。染毒组和时间观察组连续静式吸入1，2-DCE12h，对照组不接触1，2-DCE和其他化学物。染毒组接触剂量分别为5．0、10．0、20．0g／m^3，时间观察组接触剂量均为10．0g／m^3，染毒结束后在干净无毒的环境中分别放置2、4、6h；NMDAR1在大鼠脑组织中的表达采用免疫组织化学法检测。结果NMDAR1阳性神经元主要分布在大脑皮质和海马。阳性细胞百分比结果：（1）10．0、20．0g／m^3剂量组表达量高于对照组，差异有统计学意义（P〈0．05）。大脑皮质分别为（18．33±1．86）％、（64．17±2．86）％，对照组（1．83±0．75）％；海马分别为（15．5±1．87）％、（47．83±2．16）％，对照组（0．83±0．75）％；（2）时间观察组表达量：大脑皮质2、4、6h组高于对照组和10．0g／m^3剂量组，差异有统计学意义（P〈0．05）；表达量分别为（39．07±3．01）％、（70．17±2．93）％、（39．83±2．32）％。海马2、4、6h组也高于对照组，表达量分别为（16．30±1．03）％、（19．80±1．17）％、（16．50±1．05）％，差异有统计学意义（P〈0．05）；但与10．0g／m^3剂量组比较，仅4h组有明显增加，差异有统计学意义（P〈0．05）。结论1，2-DCE急性中毒过程中，NMDAR1表达数量明显上调，兴奋性氨基酸可能通过大量NMDAR1的快速开放参与脑皮质细胞的急性肿胀过程，加重脑水肿的发生。Objective： To study the role of N-methyl-D-aspartate receptor-1 in acute intoxicated encephalopathy induced by 1,2-dichloroethane（1,2-DCE）. Methods Forty-two Sprague-Dawley rats, which had been randomly divided into 1 control, 3 exposure and 3 after-exposure observation groups, were exposed to 1,2- DCE for 12hr by continual static inhalation except control group. Dosage of exposure groups was 5.0,10.0, 20.0 g/m^3 on sequence. That of after-exposure observation groups was 10.0 g/m^3. Rats of after-exposure observation groups were observed continually for 2, 4, 6 hr after exposure. The expression of N-methyl-D-aspartate receptor-1 （NMDAR1） was detected by immunohischemical method. Results NMDAR1 stained neurons were mainly distributed at cerebral cortex and hippocampus. Compared with that of control group, the percentages of positive cells of NMDAR1 increased significantly in 10.0, 20.0 g/m^3 groups （P〈0.05）. They were （18.33± 1.86）%, （64.17±2.86）% at cerebral cortex, （15.5±1.87）%, （47.83±2.16）% at hippocampus. The percentages were also elevated obviously in 2, 4, 6 h after-exposure observation groups. They were （39.07±3.01）%, （70.17±2.93）%, （39.83±2.32）% at cerebral cortex, （16.30±1.03）%, （19.80±1.17）%, （16.50±1.05）% at hippocampus; Compared with that of 10.0 g/m^3 group, the percentages increased significantly only in 4hr group at hippocampus. Conclusion The overactivation of NMDAR1 is the main route by which excitatory amino acids choose to join the development of acute intoxicated encephalopathy induced by 1, 2-DCE.

关 键 词：二氯乙烷类 中毒性脑病 N-甲基-D-天冬氨酸 Ⅰ型受体 

分 类 号：R686[医药卫生—骨科学]