Abstract—In an experimental model of Parkinson’s disease, the dopamine content in the striatum, the density of TH+ neurons in the substantia nigra, and the motor activity of mice were studied after the administration of afobazole, which interacts with Sigma-1 and MT₁ receptors and regulatory sites of MAO-A and quinone reductase 2 (NQO2, MT₃ receptor), and its main metabolite M-11, which selectively interacts only with the regulatory site of NQO2. The drugs were administered intraperitoneally for 14 days with the start of the course 30 minutes after unilateral intrastriatal administration of 5 μg of 6‑hydroxydopamine (6‑OHDA). Afobazole and M‑11 showed neuroprotective properties. In all experiments, the effective dose of afobazole (2.5 mg/kg) was significantly lower than M-11 (7.5 mg/kg). The experimental model used shows the contribution of NQO2 and other drug targets to the antiparkinsonian effect of afobazole.

中文翻译：

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喹诺酮还原酶2的作用与Afobazole抗帕金森病作用的机制分析

摘要—在帕金森氏病的实验模型中，研究了阿福巴唑与Sigma-1和MT ₁相互作用后，纹状体中的多巴胺含量，黑质中TH +神经元的密度以及小鼠的运动活动。受体和MAO-A和醌还原酶2（NQO2，MT _3的调节位点受体）及其主要代谢物M-11（仅与NQO2的调节位点选择性相互作用）。在单侧纹状体内注射5μg6-羟基多巴胺（6-OHDA）后30分钟的疗程开始，腹膜内给药14天。Afobazole和M-11具有神经保护作用。在所有实验中，阿福唑的有效剂量（2.5 mg / kg）显着低于M-11（7.5 mg / kg）。所使用的实验模型表明NQO2和其他药物靶标对阿夫巴唑的抗帕金森效应有贡献。