摘要
目的研究神经细胞黏附分子(neural cell adhesion molecule,NCAM)在胶质细胞系源性神经营养因子(glial cell line-derived neurotrophic factor,GDNF)保护帕金森(Parkinson's disease,PD)模型大鼠受损多巴胺(dopamine,DA)能神经元中的作用。方法右侧纹状体内立体定位注射6-羟多巴胺(6-OHDA)制备早期PD模型,而后分为4组:对照组(同侧黑质内注射PBS)、NCAM组(同侧黑质内仅注射anti-NCAM抗体)、GDNF组(同侧黑质内注射GDNF)、NCAM阻断组(同侧黑质内注射anti-NCAM抗体30min后注射GDNF),采用免疫组织化学染色技术和免疫印迹技术,观察各组酪氨酸羟化酶(tyrosine hydroxylase,TH)的表达变化。结果GDNF组黑质致密部TH阳性神经元数目及表达的量明显多于PBS组,差别有统计学意义;NCAM阻断组与GDNF组相比,该处TH阳性神经元数目及表达的量明显减少,差别有统计学意义。结论NCAM参与了GDNF保护DA能神经元的作用。
Objective To explore whether neural cell adhesion molecule （NCAM） mediates the protective el-fect of glial cell line-derived neurotrophic factor（GDNF） on injured dopaminergic （DA） neurons. Methods The early period of Parkinson＇s disease（PD）models were established by stereotaxic injection of 6-OHDA. The rats were divided into 4 groups respectively ：control group, NCAM group ,GDNF group ,and GDNF＋anti-NCAM group. Immunohistochemistry and Western blot were used to examine the number of TH-positive cells and the expresse level of TH protein in SN of rat. Results GDNF significantly increased the number of TH-positive cells and the ex- pressing of TH as compared to control group. However,when the NCAM pathway was blocked by injecting anti NCAM,the number of TH positive cells and the level of TH were significantly decreased. Conclusion GDNF protects the injured DA neurons,and NCAM may be involved in protective effect of GDNF on DA neurons.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2007年第4期428-430,共3页
Journal of Apoplexy and Nervous Diseases
基金
国家自然科学基金资助项目(No.30570564)
