蛋白激酶Cδ参与帕金森大鼠模型中6-OHDA的神经毒性作用

发布时间：2018-04-29 14:49

本文选题：-羟基多巴胺 + 帕金森病　；参考：《中风与神经疾病杂志》2017年11期

【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(P0.05);Western blotting显示PD组SNpc组织中PKCδ及Cleaved PKCδ的表达较Sham组显著上调(P0.05);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。
[Abstract]:Objective to study the role of protein kinase C 未 (PKC 未) in neuronal loss in Parkinson's model. Methods Forty male Sprague-Dawley rats were randomly divided into Sham group (n = 10) and PD group (n = 30). The right striatum was injected with normal saline or 6-OHDA solution and rotated by apomorphine. The expression of tyrosine hydroxylase (THH) in the dense part of substantia nigra was detected by immunohistochemistry. The expression of PKC 未 protein was detected by Western blotting and the expression of PKC 未 in nucleus was observed by confocal method. Results the histopathological changes of th positive neurons were observed in the SNpc site of PD group and the density decreased significantly. The expression of PKC 未 and Cleaved PKC 未 in SNpc tissue of PD group was significantly up-regulated than that in Sham group, and the confocal microscope indicated that PKC 未 and Cleaved PKC 未 in SNpc were significantly up-regulated in PD group. The nucleus is colocated. Conclusion the enzymatic activation and nuclear translocation of PKC 未 may be involved in the neuropathology of PD.
【作者单位】：贵州医科大学地方病与少数民族疾病教育部重点实验室贵州省医学分子生物学重点实验室贵州医科大学分子生物学重点实验室;贵州医科大学生物学教研室;贵州医科大学附院神经内科;贵州医科大学病理学教研室;
【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)
【分类号】：R-332;R742.5

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