CAJ | 학술논문

向大鼠侧脑室内注射聚集态的β-淀粉样多肽(Aβ 25-35)15mmol后，动物在三种行为试验中都出现学习记忆障碍，同时海马和大脑皮层的胆碱乙酰转移酶(ChAT)活性下降。这表明应用Aβ 25-35脑室内注射造成Alzheimer’s病动物模型的可行性。764-3于手术后早期多次给药(2mg/0.5mL　每天1次i.p.)明显改善Aβ 25-35所致的学习记忆缺陷，并使海马的ChAT回升。本文又首次报告Aβ 25-35引起前脑多个脑区的一氧化氮合酶(NOS)表达上调，764-3拮抗此反应。结果提示764-3的作用机制与其在脑内提高ChAT活性和抑制病理性的NOS表达有关。
향대서측뇌실내주사취집태적β-정분양다태(Aβ 25-35)15mmol후，동물재삼충행위시험중도출현학습기억장애，동시해마화대뇌피층적담감을선전이매(ChAT)활성하강。저표명응용Aβ 25-35뇌실내주사조성Alzheimer’s병동물모형적가행성。764-3우수술후조기다차급약(2mg/0.5mL　매천1차i.p.)명현개선Aβ 25-35소치적학습기억결함，병사해마적ChAT회승。본문우수차보고Aβ 25-35인기전뇌다개뇌구적일양화담합매(NOS)표체상조，764-3길항차반응。결과제시764-3적작용궤제여기재뇌내제고ChAT활성화억제병이성적NOS표체유관。
Intracerebroventricular (icv) administration of aggregated beta-amyloid peptide 25-35(Aβ 25-35, 15nmol) in rats induced learning and memory impairment in three behavioral tasks. Meanwhile, activity of choline-acetyltransferase (ChAT) in hippocampus and cerebral cortex reduced. This demonstrates that Aβ 25-35 (icv) injection to produce a rat model for Alzheimers disease is feasible. Post-surgery repeated treatment of 764-3 (2mg/day i.p.) significantly improved learning and memory deficits caused by Aβ 25-35 and increased ChAT activity in hippocampus. Moreover, present study reported, for the first time, that Aβ 25-35 (icv) induced up-expression of nitric oxide synthase (NOS) in several areas of forebrain and 764-3 blocked this response. Results suggest that mechanism of 764-3 treatment involves rise of ChAT activity and depression of NOS pathological expression in the brain.