In Parkinson's disease (PD), degradation of dopaminergic neurons in substantia nigra causes striatal deficiency of dopamine, which results in tremors, bradykinesia with instability in posture, rigidity and shuffled gait. Prevalence of PD increases with age as from 65 to 85 years. In an attempt to devise targeted safe therapy, nanoparticles of methyl 4-hydroxy-2H-1,2-benzothiazine-3-carboxylate 1,1-dioxide (MBD) (MBDN), were prepared and their acute toxicity and safety was evaluated. Thirty-six healthy albino mice were randomly divided into six groups (n = 6): normal control, diseased control, standard (levodopa/carbidopa (100/25 mg/kg) and the remaining three groups were administered 1.25, 2.5 and 5 mg/kg MBDN during 21 days study. Except control, all mice, were injected haloperidol (1 mg/ kg i.p.) 1-h prior to treatment to induce PD. Acute toxicity test showed, no effect of MBDN on lipid profile, brain, renal and liver function and histoarchitecture of kidney, liver and heart, except decreased (p < 0.05) platelet count. Behavioral studies showed significant improvement (p < 0.001) in motor function and reduction of oxidation status in a MBDN in a dose dependent manner. Thus, the study findings revealed significance of MBDN as a selective MAO-B inhibitor for the improvement of Parkinson's symptoms in animal model.

在帕金森病 (PD) 中，黑质中的多巴胺能神经元退化导致纹状体缺乏多巴胺，从而导致震颤、运动迟缓、姿势不稳定、僵硬和步态拖沓。PD 的患病率随着年龄从 65 岁到 85 岁而增加。为了设计有针对性的安全疗法，制备了甲基4-羟基-2H-1,2-苯并噻嗪-3-羧酸酯1,1-二氧化物（MBD）（MBDN）纳米颗粒，并评估了其急性毒性和安全性。36只健康白化小鼠随机分为六组（ n = 6）：正常对照、患病对照、标准（左旋多巴/卡比多巴（100/25 mg/kg）），其余三组分别给予1.25、2.5和5 mg在21天的研究中，除对照组外，所有小鼠均在治疗前1小时注射氟哌啶醇（1 mg/ kgip）诱导PD。急性毒性试验显示，MBDN对血脂、脑、肾功能和肝功能以及肾、肝和心脏的组织结构，除了血小板计数减少 (p ，MBDN 的运动功能显着 改善 (p因此，研究结果揭示了 MBDN 作为选择性 MAO-B 抑制剂对于改善动物模型帕金森症状的重要性。