中文摘要：

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，^22 P-特异底物标记技术检测PP-2A活性。砖果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VitE；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。

英文摘要：

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.