CAJ | 학술논문

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/LOA与PC12共培养48小时，NOS活性轻度增强；当增加OA浓度至10nmol/L时，培养24和48小时均可见NOS活性明显增强。结果表明根据1nmol/LOA抑制蛋白磷酸酶(PP)-2A，而10nmol/LOA除完全抑制PP-2A外，还部分抑制PP-1，提示PP-2A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AD的关系和作用有待继续研究。
단백린산매강저삼여아이자해묵병(AD)신경원퇴화，본문지재탐토일양화담(NO)재tau단백과도린산화인기AD뇌신경원퇴화중적가능작용。채용β-환원형니극선알선표령이핵감산린산-황체매(β-NADPH-d)조직화학기술연구불동제량단백린산매억제제강전산(OA)대기락세포류세포주(PC12)일양화담합성매(NOS)활성적영향。결과현시1nmol/LOA여PC12공배양48소시，NOS활성경도증강；당증가OA농도지10nmol/L시，배양24화48소시균가견NOS활성명현증강。결과표명근거1nmol/LOA억제단백린산매(PP)-2A，이10nmol/LOA제완전억제PP-2A외，환부분억제PP-1，제시PP-2A화PP-1적억제균가증강NOS활성사NO산생증가。관우단백린산매활성강저화NO산생증다여AD적관계화작용유대계속연구。
To determine the relationship between the activity of NOS and thelow 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.