【摘要】 目的　探讨抑制褪黑素的生物合成对大鼠海马神经细丝过度磷酸化的影响及其可能机制。方法　侧脑室注射氟哌啶醇并腹腔注射加强 ,HPLC检测血清中褪黑素水平 ;利用免疫组化检测大鼠海马区域神经细丝磷酸化情况 ;微量测定法测定超氧化物歧化酶 (SOD)活性和脂质过氧化产物丙二醛的含量。结果　①模型组大鼠血清中褪黑素的含量明显下降。②海马区域神经细丝发生聚集和异常过度磷酸化 ,补充不同剂量的褪黑素的治疗组较模型组的磷酸化程度有所改善。③模型组SOD活性降低 ,丙二醛 (MDA)含量明显升高。结论　褪黑素水平的降低引起AD 样神经细丝异常过度磷酸化 ,外源性补充褪黑素可以一定程度上减轻神经细丝的异常过度磷酸化。更多还原

【Abstract】 ? Objective To investigate the in vivo effect of inhibiting melatonin biosynthesis onneurofilament(NF) phosphorylationinrats. Method Lateral ventricular and intraperitonealinjection was used for administering haloperidol,HPLC for detectingthe level of melatonin in serum, immunohistochemistry for measuring phosphorylation of NF, and spectrophotometry for examining the activity of SOD and the content of MDA. Result Abnormal hyperphosphorylation of NF was found in the hippocampuswhen the biosynthesisof melatoninwas inhibited, while melatonin supplement attenuated this phosphorylation. Conclusion Decreased melatonin may be involved in Alzheimer-like NF hyperphosphorylation, and supplement of melatonin attenuates this abnormality.更多还原