氯化甲基汞对发育阶段大鼠小脑PKCδmRNA及蛋白表达的影响  

Effects of Methylmercury chloride exposure on PKCδ expression in rat developmental cerebellum

作　　者：张宏宇[1] 刘忠山[2] 王铁君[2] 李志超[3] 郭杰[2] 

机构地区：[1]中国人民解放军208医院461临床部,长春130061 [2]吉林大学第二医院放疗科,长春130041 [3]吉林大学公共卫生学院,长春130061

出　　处：《中国免疫学杂志》2016年第8期1192-1194,共3页Chinese Journal of Immunology

基　　金：吉林省卫生厅科研基金资助项目(3D5097923427);吉林大学基本科研业务费专项基金资助项目(421030140427);吉林大学青年教师基金资助项目(419070210048)

摘　　要：目的:观察氯化甲基汞对发育大鼠小脑中PKCδmRNA及蛋白表达的影响。方法:建立发育大鼠小脑甲基汞损伤实验模型。采用核酸原位杂交方法(In Situ Hybridization,ISH)检测δ型蛋白激酶C(PCKδ)mRNA表达。采用Western blot方法检测PKCδ蛋白表达。结果:实验组和对照组仔鼠在出后就即可检测到小脑蒲肯野细胞PKCδ表达,且随生后时间延长表达水平虽有增高但幅度很小。各实验组仔鼠脑汞含量明显高于对照组,且实验组小脑蒲肯野神经元PKCδmRNA表达阳性率及小脑组织胞浆和胞膜PKCδ蛋白表达水平显著升高(P<0.05)。结论:氯化甲基汞以剂量依赖方式和时间依赖方式促进仔鼠小脑蒲肯野细胞PKCδmRNA及蛋白表达。PKCδ亚类可能是甲基汞介导神经毒作用的关键靶分子。Objective： To investigate the effect of Methylmercury chloride chronic exposure on PKCδ expression developing cerebellum. Methods： Establishment of cerebellum damage model of developmental rats by chronic MMC exposure. In Situ Hybridization and Western blot analysis were performed to detect the expression of PKC isozyme. Results： PKCδ was expressed at high levels at birth,but no significant change was observed with the increase in the time of birth corresponding to brain Hg^2 ＋level,expression of PKCδ in cerebellum of experimental groups was markedly higher than that of control group. Conclusion： Neurotoxicity of Methylmercury chloride exposure might be mediated by PKCδ expression up-regulating in developmental cerebellum.

关 键 词：氯化甲基汞 脑发育 PKCΔ expression 

分 类 号：R135.13[医药卫生—劳动卫生]