Introduction: The leading cause of memory impairment is dementia-related disorders. Since current treatments for memory impairment target the neuroinflammatory pathways, we selected dapsone, an anti-inflammatory agent, to evaluate its effects on scopolamine-induced memory impairment in mice and the underlying role of nitric oxide (NO). Methods: Scopolamine (1 mg/kg, intraperitoneal [i.p.]) was used for induction of memory impairment. The animals received various doses of dapsone (0.1, 0.3, 1, 5, and 10 mg/kg, i.p.). Duration and number of arms visits in the Y-maze and step-through latency in the passive-avoidance were documented. To evaluate the underlying signaling pathway, N(ω)-nitro-L-arginine methyl ester (a nonspecific NO synthase [NOS] inhibitor), aminoguanidine (a specific inducible NOS inhibitor), and 7-nitroindazole (a specific neuronal NOS inhibitor) were administered 30 min after dapsone administration. Results: Dapsone (5 mg/kg) substantially improved memory acquisition in scopolamine-induced memory impairment. Additionally, NOS inhibitors considerably reversed the observed neuroprotective effects of dapsone, accompanied by the elevation of NO levels. Conclusion: Dapsone revealed a neuroprotective effect against scopolamine-induced memory impairment in mice, possibly through the nitrergic pathway.
Dement Geriatr Cogn Disord Extra 2022;12:43–50

中文翻译：

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氨苯砜对东莨菪碱诱导的小鼠记忆障碍的保护作用：一氧化氮通路的参与

简介：记忆障碍的主要原因是痴呆相关疾病。由于目前对记忆障碍的治疗以神经炎症途径为目标，我们选择氨苯砜，一种抗炎剂，以评估其对东莨菪碱诱导的小鼠记忆障碍的影响以及一氧化氮 (NO) 的潜在作用。方法：东莨菪碱（1 mg/kg，腹膜内[ip]）用于诱导记忆障碍。动物接受不同剂量的氨苯砜（0.1、0.3、1、5和10mg/kg，ip）。记录了 Y 形迷宫中手臂访问的持续时间和数量以及被动回避中的逐步潜伏期。为了评估潜在的信号通路，N(ω)-硝基-L-精氨酸甲酯（一种非特异性 NO 合酶 [NOS] 抑制剂）、氨基胍（一种特异性诱导型 NOS 抑制剂）和 7-硝基吲唑（一种特异性神经元 NOS 抑制剂）氨苯砜给药后 30 分钟给药。结果：氨苯砜 (5 mg/kg) 显着改善了东莨菪碱引起的记忆障碍的记忆获取。此外，NOS 抑制剂显着逆转了观察到的氨苯砜的神经保护作用，伴随着 NO 水平的升高。结论：氨苯砜对东莨菪碱引起的小鼠记忆障碍具有神经保护作用，可能是通过氮能途径。
Dement Geriatr Cogn Disord Extra 2022；12：43–50