摘要
目的研究蛋白激酶Cδ(PKCδ)细胞核转移在帕金森大鼠模型神经元丢失中的病理作用。方法 40只雄性SD大鼠随机分为Sham组(10只)和PD组(30只),立体定位右侧纹状体注射生理盐水或6-OHDA溶液并通过阿朴吗啡(APO)诱导旋转进行模型筛选,免疫组化检测黑质致密部(SNpc)酪氨酸羟化酶(TH)表达情况。采用Western blotting检测PKCδ蛋白表达并通过共聚焦观察PKCδ在细胞核的表达。结果 PD组SNpc部位TH阳性神经元形态发生了病理改变且密度显著下降(P<0.05);Western blotting显示PD组SNpc组织中PKCδ及Cleaved PKCδ的表达较Sham组显著上调(P<0.05);共聚焦显微镜提示PD组SNpc部位PKCδ与细胞核有共定位。结论 PKCδ的酶解激活及细胞核转位可能参与了PD的神经病理发生。
Objective To investigate the pathological role of proteolytic activation of protein kinase Cδ（PKCδ） in the loss of dopaminergic neurons in rat model of Parkinson＇s disease（PD）. Methods 40 male SD rats were randomly divided into Sham group（10） and PD group（30）. All rats were stereotacticly injected by saline or 6-OHDA solution,and screened by Apomorphine（APO） induced rotation. Immunohischemical staining was adopted to observe the positive neurons of tyrosine hydroxylase（TH） in substantia nigra pars compacta（SNpc）. The expression of PKCδ was detected by Western blotting; the translocation of PKCδ into nucleus was detected by confocal microscope. Results Immunohischemistry showed the pathological change of TH positive neurons and its significant decrease in SNpc of PD（P 0. 05）; Western blotting showed that the expression of PKC δ and Cleaved PKC δ were significantly upregulated in SNpc of PD（P 0. 05）;confocal microscope showed localization of PKC δ in nucleus in the SNpc of PD. Conclusion Proteolytic activation and nucleus translocation of PKC δ were possibly involved in the neuropathogenesis of PD.
出处
《中风与神经疾病杂志》
北大核心
2017年第11期969-972,共4页
Journal of Apoplexy and Nervous Diseases
基金
国家自然科学基金(No.81360199)
教育部科学技术研究项目(No.213032A)
贵州省国际科技合作计划项目{黔科合外G字[2013]7026}
贵州省创新计划项目{黔教合协同创新中心[2014]06}
贵州省教育厅项目(2015年贵州省普通高等学校地方病和少数民族疾病防控创新团队)
关键词
6-羟基多巴胺
帕金森病
蛋白激酶Cδ
转位
6-Hydroxydopamine Parkinson’s disease
Protein kinase Cδ
Translocation
