Department of Biochemistry and Molecular Biology, Faculty of Medicine, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Cordoba, Spain.
Pharmacol Rep. 2013;65(3):624-31. doi: 10.1016/s1734-1140(13)71039-9.
Natalizumab is a monoclonal antibody used to treat multiple sclerosis. This study sought to determine whether the protective action of natalizumab involved a reduction in oxidative damage.
Twenty-two multiple sclerosis patients fulfilling the revised McDonald criteria were assigned to treatment with 300 mg natalizumab intravenously once monthly (infusion every 4 weeks) in accordance with Spanish guidelines. Carbonylated proteins, 8-hydroxy-2'-deoxyguanosine, total glutathione, reduced glutathione, superoxide dismutase, glutathione peroxidase, and myeloperoxidase levels were measured at baseline and after 14 months' treatment, and the antioxidant gap was calculated.
Natalizumab prompted a drop in oxidative-damage biomarker levels, together with a reduction both in myeloperoxidase levels and in the myeloperoxidase/neutrophil granulocyte ratio. Interestingly, natalizumab induced nuclear translocation of Nrf2 and a fall in serum vascular cell adhesion molecule-1 levels.
These findings suggest that natalizumab has a beneficial effect on oxidative damage found in MS patients.
那他珠单抗是一种用于治疗多发性硬化症的单克隆抗体。本研究旨在确定那他珠单抗的保护作用是否涉及氧化损伤的减少。
根据西班牙指南,将 22 名符合修订后的麦克唐纳标准的多发性硬化症患者分配接受每月一次(每 4 周输注一次)静脉内 300mg 那他珠单抗治疗。在基线和治疗 14 个月后测量羰基蛋白、8-羟基-2'-脱氧鸟苷、总谷胱甘肽、还原型谷胱甘肽、超氧化物歧化酶、谷胱甘肽过氧化物酶和髓过氧化物酶水平,并计算抗氧化剂间隙。
那他珠单抗降低了氧化损伤生物标志物水平,同时降低了髓过氧化物酶水平和髓过氧化物酶/中性粒细胞粒细胞比值。有趣的是,那他珠单抗诱导 Nrf2 的核转位和血清血管细胞黏附分子-1 水平的下降。
这些发现表明,那他珠单抗对多发性硬化症患者的氧化损伤有有益的影响。