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机构地区:[1]三峡大学医学院病理生理教研室,湖北宜昌443002 [2]华中科技大学同济医学院病理生理教研室,湖北武汉430030
出 处:《西安交通大学学报(医学版)》2006年第2期123-126,共4页Journal of Xi’an Jiaotong University(Medical Sciences)
基 金:国家自然科学基金资助项目(No.30170221No.30100057)
摘 要:目的探讨褪黑素(Mel)对花萼海绵诱癌素(CA)在成神经瘤细胞诱导的神经细丝过度磷酸化中的影响及其机制。方法采用鼠野生型成神经瘤细胞(N2awt),给予CA处理,或同时给予不同浓度Mel或维生素E(Vit E)处理,并用免疫印迹法检测神经细丝磷酸化水平和蛋白磷酸酯酶2A(PP-2A)含量,32P-特异底物标记技术检测PP-2A活性。结果①CA可在N2awt细胞引起神经细丝过度磷酸化,同时伴有PP-2A含量和活性降低。②Mel对CA引起的神经细丝过度磷酸化有保护作用,且强于Vit E;Mel同时对抗CA诱导的PP-2A活性和含量降低。结论Mel可通过调节细胞内PP-2A的含量和活性而减轻CA引起的神经细丝过度磷酸化。Objective To investigate the in vivo effect of melatonin on calyculin A-induced neurofilament (NF) hyperphosphorylation in neuroblastma cells (N2awt). Methods N2awt cells were treated with CA or CA and different concentration melatonin or CA and vitamin E, the levels of neurofilament phosphorylation and the level of PP-2A were detected, and the activities of PP-2A were assayed. Results Calyculin A treatment led to neurofilament hyperphosphorylation by decreasing the level and activity of PP-2A. Both melatonin and vitamin E had protective effect on calyculin A-induced neurofilament hyperphosphorylation, although melatonin increased the activity of PP-2A while vitamin E did not. Morever, melatonin partially attenuated the decreasing of PP-2A level. Conclusion Melatonin protects neuroblastma cells from CA-induced neurofilament hyperphosphorylation through the regulation of PP-2A level and the increase of PP-2A activity.
关 键 词:阿尔茨海默病 花萼海绵诱癌素 褪黑素 神经细丝 过度磷酸化
分 类 号:R745.7[医药卫生—神经病学与精神病学] Q513[医药卫生—临床医学]
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