凋亡调节蛋白在蛋白磷酸酶抑制剂所诱导的大鼠脑神经细胞退化中的表达分析  

EXPRESSION OF APOPTOTIC REGULATED PROTEIN IN DEGENERATED NEURONS WAS INDUCED BY AN INHIBITOR FOR PROTEIN PHOSPHATASE IN RAT BRAIN

作　　者：陈丽琴[1] 刘萨日娜[1] 苏丽娟[1] 

机构地区：[1]内蒙古医学院基础医学院,内蒙古呼和浩特010059

出　　处：《内蒙古医学院学报》2008年第5期326-331,共6页Acta Academiae Medicinae Neimongol

基　　金：内蒙古医学院博士启动基金项目(NY2006BQ002)

摘　　要：目的:在体内水平探讨凋亡调节蛋白Bcl-2/Bax在蛋白磷酸酶抑制剂冈田酸所致的神经细胞退化中的表达情况及其影响。方法:采用大鼠脑皮质定位注射冈田酸的模型,应用免疫组化染色法检测冈田酸所诱导的Bcl-2和Bax蛋白表达情况,用图像分析技术和光学显微镜测微网格分别计数Bcl-2和Bax免疫阳性细胞。结果:Bcl-2和Bax蛋白在大鼠脑额叶皮质有广泛性的基础表达,冈田酸能特异性诱导Bcl-2和Bax蛋白高表达,相邻平面脑片的Bcl-2免疫阳性细胞的分布范围和细胞数目大于和多于Bax免疫阳性细胞。结论:冈田酸诱导凋亡相关调节蛋白Bcl-2和Bax高表达,提示Bcl-2/Bax相关凋亡调节机制参与冈田酸所致神经细胞退化过程;Bcl-2阳性细胞的分布范围和细胞数目大于和多于Bax阳性细胞,提示神经细胞可能存在内在抗损伤机制增加对冈田酸所致损伤的耐受性。Objective：To explore the effect of Bcl -2/Bax regulated apoptotic mechanism on neuronal degeneration induced by Okadaic acid （ OA）, an inhibitor for protein phosphatase, in vivo Methods： A model of microinjection of OA was applied in the study. Immunohistochemistry was used for examining expression of Bcl - 2 and Bax protein in rat brain injected by OA. Bcl - 2 - and Bax - positive ceils were counted by means of image processing/analysis system and 400 × light microscopy, respectively. Results： Bcl - 2 and Bax protein was widely expressed in rat frontal cortex at a basic level. OA induced high expression of Bcl -2 and Bax protein specially surrounding the injection site. In the closely adjacent level brain slices, distribution range of Bcl - 2 - positive cells was larger than that of Bax - positive cells; Number of Bcl - 2 - positive cells was more than that of Bax - positive cells Conclusion ：These results suggested that Bcl -2/Bax regulated mechanism was involved in neuronal degeneration induced by OA and that protective mechanism was possibly existed in neurons to antagonize the damage induced by OA.

关 键 词：BCL-2蛋白 BAX蛋白 阿尔茨海默病 蛋白磷酸酶抑制剂 冈田酸 

分 类 号：R31[医药卫生—基础医学]