Center for Neuroimmunology, Institut d'Investigacions Biomediques August Pi Sunyer, Casanova 145, Centre Cellex 3A, 08036, Barcelona, Spain.
Institute for Advanced Chemistry of Catalonia, Consejo Superior de Investigaciones Cientificas, Barcelona, 08034, Spain.
Neurotherapeutics. 2019 Jul;16(3):808-827. doi: 10.1007/s13311-019-00717-4.
The development of neuroprotective therapies is a sought-after goal. By screening combinatorial chemical libraries using in vitro assays, we identified the small molecule BN201 that promotes the survival of cultured neural cells when subjected to oxidative stress or when deprived of trophic factors. Moreover, BN201 promotes neuronal differentiation, the differentiation of precursor cells to mature oligodendrocytes in vitro, and the myelination of new axons. BN201 modulates several kinases participating in the insulin growth factor 1 pathway including serum-glucocorticoid kinase and midkine, inducing the phosphorylation of NDRG1 and the translocation of the transcription factor Foxo3 to the cytoplasm. In vivo, BN201 prevents axonal and neuronal loss, and it promotes remyelination in models of multiple sclerosis, chemically induced demyelination, and glaucoma. In summary, we provide a new promising strategy to promote neuroaxonal survival and remyelination, potentially preventing disability in brain diseases.
神经保护疗法的开发是一个备受关注的目标。通过使用体外检测方法对组合化学文库进行筛选,我们发现了小分子 BN201,它可以促进培养的神经细胞在受到氧化应激或缺乏营养因子时的存活。此外,BN201 还可以促进神经元分化、前体细胞向体外成熟少突胶质细胞的分化以及新轴突的髓鞘形成。BN201 调节参与胰岛素样生长因子 1 通路的几种激酶,包括血清糖皮质激素激酶和中期因子,诱导 NDRG1 的磷酸化和转录因子 Foxo3 向细胞质的易位。在体内,BN201 可以防止轴突和神经元的丢失,并促进多发性硬化症、化学诱导的脱髓鞘和青光眼模型中的髓鞘再生。总之,我们提供了一种新的有前途的策略来促进神经轴突的存活和髓鞘再生,从而有可能预防脑部疾病导致的残疾。