磷酸化ERK1/2在6-OHDA致PC12细胞损伤中的作用  

Effect of phosphorylation of ERK1/2 on PC12 cell injury induced by 6-OHDA

作　　者：李静[1] 张一娜[1] 范鹰[1] 马兰[1] 姜礼红[1] 崔璨[1] 吴博[2] 

机构地区：[1]哈尔滨医科大学附属第二医院老年病科,黑龙江哈尔滨150086 [2]哈尔滨医科大学病理生理教研室

出　　处：《中国老年学杂志》2012年第15期3244-3246,共3页Chinese Journal of Gerontology

基　　金：黑龙江省卫生厅科研课题(No.2009-131);黑龙江省教育厅科学技术项目(No.11521076;No.11551213);黑龙江省科技厅国际合作项目(No.WB08B05)

摘　　要：目的观察细胞外信号调节激酶(ERK1/2)在6-OHDA致PC12细胞损伤的帕金森(PD)细胞模型中所起的作用。方法 6-OHDA处理体外培养的PC12细胞株,建立PD细胞模型。MTT法检测6-OHDA对PC12细胞活力的影响,免疫印迹法研究p-ERK1/2蛋白表达随时间变化的趋势,并检测ERK1/2上游激酶抑制剂PD98059和U0126对6-OHDA诱导ERK1/2磷酸化及凋亡的影响。结果 PC12细胞随6-OHDA作用时间的增加,p-ERK1/2出现表达升高;PD98059和U0126明显抑制6-OHDA所致的ERK1/2磷酸化,明显减低了细胞损伤的程度。结论在6-OHDA介导的多巴胺神经元损伤中呈现ERK1/2磷酸化,抑制ERK1/2可以6-OHDA引起的PC12细胞损伤,该过程可能在调控PD多巴胺能细胞损伤中起重要作用。Objective To observe the effect of extracellular signal-regulated kinase （ERK1/2） in PC12 cell injury induced by 6- OHDA. Methods 6-OHDA treatment of PC12 cells in vitro was established to make Parkinson＇s disease （PD） cell model. MTT assay was used to observe cell viability, Western blotting was used to detect p-ERK1/2 protein expression, and ERK1/2 upstream kinase inhibitors PD98059 and U0126 effect on t ERK1/2 phosphorylation and apoptosis induced by 6-OHDA. Results With time increasing, p-ERK1/2 ex- pression elevated, PD98059 and U0126 significantly inhibited phosphorylation of ERK1/2 induced by 6-OHDA, reduced the degree of PC12 cells damage. Conclusions Phosphorylation of ERK1/2 existed in the 6-OHDA induced PC12 cells injury, inhibition of ERK1/2 phospho- rylation with PD98059 and U0126 may ameliorate the injury of 6-OHDA induced PC12 cells, which may play an important role in the regula- tion of PD dopaminergic cells injury.

关 键 词：PC12细胞 PD98059 U0126 帕金森病 ERK1/2 

分 类 号：R742.5[医药卫生—神经病学与精神病学]