Liang Li-Ping, Fulton Ruth, Bradshaw-Pierce Erica L, Pearson-Smith Jennifer, Day Brian J, Patel Manisha
Department of Pharmaceutical Sciences, University of Colorado, Anschutz Medical Campus, Aurora, Colorado (L.-P.L., R.F., E.-L.B.-P., J.P.-S., B.J.D., M.P.) and Department of Medicine, National Jewish Health, Denver, Colorado (B.J.D.).
Department of Pharmaceutical Sciences, University of Colorado, Anschutz Medical Campus, Aurora, Colorado (L.-P.L., R.F., E.-L.B.-P., J.P.-S., B.J.D., M.P.) and Department of Medicine, National Jewish Health, Denver, Colorado (B.J.D.)
J Pharmacol Exp Ther. 2021 Apr;377(1):1-10. doi: 10.1124/jpet.120.000229. Epub 2021 Jan 26.
Oxidative stress plays a crucial role in the pathogenesis of Parkinson disease (PD), and one strategy for neuroprotective therapy for PD is to scavenge reactive species using a catalytic antioxidant. Previous studies in our laboratory revealed that pretreatment of lipophilic metalloporphyrins showed protective effects in a mouse PD model. In this study, we optimized the formulations of these metalloporphyrins to deliver them orally and tested their efficacy on disease outcomes in a second species after initiation of an insult (i.e., disease modification). In this study, a pharmaceutical formulation of two metalloporphyrin catalytic antioxidants, AEOL11207 and AEOL11114, was tested for oral drug delivery. Both compounds showed gastrointestinal absorption, achieved high plasma concentrations, and readily penetrated the blood-brain barrier after intravenous or oral delivery. AEOL11207 and AEOL11114 bioavailabilities were calculated to be 24% and 25%, respectively, at a dose of 10 mg/kg via the oral route. In addition, both compounds significantly attenuated 6-hydroxydopamine (6-OHDA)-induced neurotoxic damage, including dopamine depletion, cytokine production, and microglial activation in the striata; dopaminergic neuronal loss in the substantia nigra; oxidative/nitrative stress indices (glutathione disulfide and 3-nitrotyrosine) in the ventral midbrain; and rotation behavioral abnormality in rats. These results indicate that AEOL11207 and AEOL11114 are orally active metalloporphyrins and protect against 6-OHDA neurotoxicity 1-3 days postlesioning, suggesting disease-modifying properties and translational potential for PD. SIGNIFICANCE STATEMENT: Two catalytic antioxidants showed gastrointestinal absorption, achieved high plasma concentrations, and readily penetrated the blood-brain barrier. Both compounds significantly attenuated dopamine depletion, cytokine production, microglial activation, dopaminergic neuronal loss, oxidative/nitrative stress indices, and behavioral abnormality in a Parkinson disease rat model. The results suggest that both metalloporphyrins possess disease-modifying properties that may be useful in treating Parkinson disease.
氧化应激在帕金森病(PD)的发病机制中起着关键作用,而PD神经保护治疗的一种策略是使用催化抗氧化剂清除活性物质。我们实验室之前的研究表明,亲脂性金属卟啉预处理在小鼠PD模型中显示出保护作用。在本研究中,我们优化了这些金属卟啉的制剂以便口服给药,并在损伤引发后(即疾病修饰)在第二个物种中测试它们对疾病结局的疗效。在本研究中,测试了两种金属卟啉催化抗氧化剂AEOL11207和AEOL11114的药物制剂用于口服给药。两种化合物均显示出胃肠道吸收,达到高血浆浓度,并且在静脉内或口服给药后易于穿透血脑屏障。通过口服途径以10 mg/kg的剂量给药时,AEOL11207和AEOL11114的生物利用度分别计算为24%和25%。此外,两种化合物均显著减轻了6-羟基多巴胺(6-OHDA)诱导的神经毒性损伤,包括纹状体中的多巴胺耗竭、细胞因子产生和小胶质细胞活化;黑质中的多巴胺能神经元丢失;腹侧中脑中的氧化/硝化应激指标(谷胱甘肽二硫化物和3-硝基酪氨酸);以及大鼠的旋转行为异常。这些结果表明,AEOL11207和AEOL11114是口服活性金属卟啉,并且在损伤后1-3天预防6-OHDA神经毒性,提示具有疾病修饰特性以及PD的转化潜力。意义声明:两种催化抗氧化剂显示出胃肠道吸收,达到高血浆浓度,并且易于穿透血脑屏障。两种化合物均显著减轻了帕金森病大鼠模型中的多巴胺耗竭、细胞因子产生、小胶质细胞活化、多巴胺能神经元丢失、氧化/硝化应激指标和行为异常。结果表明,两种金属卟啉均具有疾病修饰特性,可能对治疗帕金森病有用。