摘要
蛋白磷酸酶降低参与阿尔茨海默病 (AD)神经元退化 ,本文旨在探讨一氧化氮 (NO)在 tau蛋白过度磷酸化引起 AD脑神经元退化中的可能作用。采用 β-还原型尼克酰胺腺嘌呤二核苷酸磷酸 -黄递酶 (β- NADPH- d)组织化学技术研究不同剂量蛋白磷酸酶抑制剂岗田酸 (OA)对嗜铬细胞瘤细胞株 (PC12 )一氧化氮合成酶 (NOS)活性的影响。结果显示 1nmol/ L OA与 PC12共培养 48小时 ,NOS活性轻度增强 ;当增加 OA浓度至 10 nmol/ L 时 ,培养 2 4和 48小时均可见 NOS活性明显增强。结果表明根据 1nmol/ L OA抑制蛋白磷酸酶 (PP) - 2 A,而 10 nmol/ L OA除完全抑制 PP- 2 A外 ,还部分抑制 PP- 1,提示 PP- 2 A和 PP- 1的抑制均可增强 NOS活性使 NO产生增加。关于蛋白磷酸酶活性降低和 NO产生增多与
To determine the relationship between the activity of NOS and the low protein phosphatase which might participate in neurofibrillary degeneration in AD. Rat pheochromocytoma cells were cultured with different dose of okadaic acid (OA), and the activity of nitric oxide synthase (NOS) was detected by β NADPH diaphorase histochemistry. NOS activity increased slightly after incubated the cells with 1 nmol/L OA for 48 hours and increased significantly with 10 nmol/L OA for 24 or 48 hours. Conclusions The inhibition of PP 2A and PP 1 might increase the production of NO through activation of NOS. A positive correlation between the inhibition of protein phosphatase(s) and the increase of NOS was also implied.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2001年第1期14-17,共4页
Chinese Journal of Histochemistry and Cytochemistry
基金
国家自然科学基金资助 (No.39870 76 7)
