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目的 :探讨一氧化氮合酶 (NOS)及一氧化氮 (NO)在 β淀粉样蛋白 (Aβ)神经毒性和Alzheimer病 (AD)发病机制中的介导作用。方法 :应用行为学及病理学方法 ,观察海马内注射Aβ1-40 对大鼠Y迷宫学习记忆的影响及对局部神经元的损伤作用 ;观察特异性诱导型一氧化氮合酶 (iNOS)抑制剂胍氨酸 (AG)及特异性神经元型一氧化氮合酶 (nNOS)抑制剂 7 硝基吲哚 (7 NI)腹腔注射对海马内注射Aβ1-40 神经毒性的干预。结果 :海马注射Aβ1-40 后 ,大鼠Y迷宫学习记忆能力及海马局部神经元明显受损 ,特异性iNOS抑制剂AG能够阻止Aβ1-40 海马注射对大鼠学习记忆和局部神经元的损伤作用 ,而特异性nNOS抑制剂 7 NI无此干预效应。结论 :iNOS/NO参与了在体条件下对Aβ神经毒性的介导 ,在AD发病机制中具有重要作用
AIM: To investigate the role of nitric oxide synthase (NOS) and nitric oxide (NO) in the pathogenesis of β-amyloid (Aβ) neurotoxicity and Alzheimer’s disease (AD). Methods: Using behavioral and pathological methods, we observed the effects of Aβ 1-40 injection on the learning and memory of rat Y-maze and the injury to local neurons. The effects of specific inducible nitric oxide synthase (iNOS) inhibitor Intervention of intraperitoneal injection of 7 nitroindole (7 NI), a selective neuronal nitric oxide synthase (AG) inhibitor, and neuronal nitric oxide synthase (nNOS) inhibitor, on neurotoxicity of Aβ 1-40 in hippocampus. Results: After Aβ 1-40 injection into the hippocampus, the learning and memory abilities of the Y maze and the local neurons in the hippocampus were significantly impaired. The specific iNOS inhibitor AG prevented the injury of learning and memory and local neurons in the hippocampus of rats , While the specific nNOS inhibitor 7 NI had no such effect. CONCLUSION: iNOS / NO is involved in the mediation of Aβ neurotoxicity in vivo and plays an important role in the pathogenesis of AD