摘要
目的研究胶质细胞系源性神经营养因子(glial cell line-derived neurotrophic factor,GDNF)对损伤的多巴胺(dopamine,DA)能神经元的保护作用和神经细胞黏附分子(neural cell adhesion molecule,NCAM)在这一保护过程中的影响。方法以培养的新生大鼠中脑脑片损伤模型和在体帕金森病(Parkinson disease,PD)模型作为观察对象。实验分3组:对照组(在无血清培养基内加入PBS或在体黑质内注射PBS)、GDNF组(在无血清培养基内加入GDNF或在体黑质内注射GDNF)、NCAM阻断组(在无血清培养基内于加入GDNF30 min前加anti-NCAM或在体黑质内注射GDNF 30 min前注射anti-NCAM阻断NCAM)。采用免疫组织化学染色技术和Western blot技术,观察各组钙结合蛋白D28K(calbindin D28K,CB)表达的变化。结果GDNF组黑质中CB阳性神经元数目及表达的量明显多于对照组,差别有统计学意义。NCAM阻断组上述指标与GDNF组相比无显著性差异。结论GDNF可能通过增加CB的表达而保护受损的DA能神经元,但NCAM可能未参与这一作用。
Objective To explore the protective effect of glial cell line - derived neurotrophic factor （GDNF） on injured dopaminergic （DA） neurons and the possible role of neural cell adhesion molecule （NCAM） in this protective process. Methods The study was carried out in vitro on injured cultured midbrain slices and in vivo on earlier models of Parkinson disease （PD）. The subjects were divided into 3 groups respectively ： control group, GDNF group and GDNF ＋ anti - NCAM group. Immunohistochemistry and Western blot were used to determine the number of calbindin （CB） - positive cells and the expression level of CB protein in midbrain slices and the substantia nigra of PD models. Results In the test groups, GDNF significantly increased the number of CB - positive cells and the expression of CB, as compared to that in the control group. However, when the NCAM pathway was blocked by adding anti - NCAM, no significant changes were noticed in the number of CB - positive cells or the level of CB. Conclusion GDNF may protect the DA neurons against injuries by increasing the expression of CB, but NCAM may not be involved in the process.
出处
《徐州医学院学报》
CAS
2007年第4期211-215,共5页
Acta Academiae Medicinae Xuzhou
基金
国家自然科学基金(30570564)
