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Protective Effects of Dapsone on Scopolamine-Induced Memory Impairment in Mice: Involvement of Nitric Oxide Pathway Publisher



Noroozi N1, 2 ; Shayan M1, 2 ; Maleki A1, 2 ; Eslami F1, 2 ; Rahimi N1, 2 ; Zakeri R3 ; Abdolmaleki Z4 ; Dehpour AR1, 2
Authors

Source: Dementia and Geriatric Cognitive Disorders Extra Published:2022


Abstract

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. © 2022
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