Liu Hui, Chen Jun-pao, Zhang Wan-qin
Department of Physiology, Dalian Medical University, Dalian 116027, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2002 Nov;18(4):329-32.
To investigate the causative role of nitric oxide synthase (NOS) and nitric oxide (NO) in neurotoxicity of beta-amyloid (Abeta) and the pathogenesis of Alzheimer's disease (AD).
Using behavioral and neuropathological methods, we observed the effects of Abeta(1-40) injection into hippocampi on rats learning and memory in Y maze and on the neuropathology in hippocampi. The intervention by intraperitoneal administration of aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor, and 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor, in the neurotoxicity of Abeta(1-40) was studied then.
The capability of acquisition and retrieval in Y maze and local neurons in hippocampus of the rats were impaired significantly after Abeta(1-40) injection. Intraperitoneal administration of AG, but not 7-NI, could prevent the damages caused by Abeta(1-40) injection above-mentioned.
iNOS/NO participates in the mechanisms of Abeta-induced neurotoxicity and may play an important role in the pathogenesis of AD.
研究一氧化氮合酶（NOS）和一氧化氮（NO）在β-淀粉样蛋白（Aβ）神经毒性及阿尔茨海默病（AD）发病机制中的作用。
采用行为学和神经病理学方法，观察向大鼠海马内注射Aβ（1-40）对其在Y迷宫中学习记忆能力及海马神经病理学的影响。随后研究腹腔注射选择性诱导型NOS（iNOS）抑制剂氨基胍（AG）和选择性神经元NOS（nNOS）抑制剂7-硝基吲唑（7-NI）对Aβ（1-40）神经毒性的干预作用。
注射Aβ（1-40）后，大鼠在Y迷宫中的获取和检索能力以及海马局部神经元均受到显著损害。腹腔注射AG可预防上述Aβ（1-40）注射所致的损害，而7-NI则无此作用。
iNOS/NO参与Aβ诱导的神经毒性机制，可能在AD发病机制中起重要作用。
