Recent evidence shows that aminochrome induces glial activation related to neuroinflammation. This dopamine derived molecule induces formation and stabilization of alpha-synuclein oligomers, mitochondria dysfunction, oxidative stress, dysfunction of proteasomal and lysosomal systems, endoplasmic reticulum stress and disruption of the microtubule network, but until now there has been no evidence of effects on production of cytokines and neurotrophic factors, that are mechanisms involved in neuronal loss in Parkinson’s disease (PD). This study examines the potential role of aminochrome on the regulation of NGF, GDNF, TNF-α and IL-1β production and microglial activation in organotypic midbrain slice cultures from P8 - P9 Wistar rats. We demonstrated aminochrome (25 μM, for 24 h) induced reduction of GFAP expression, reduction of NGF and GDNF mRNA levels, morphological changes in Iba1⁺ cells, and increase of both TNF-α, IL-1β mRNA and protein levels. Moreover, aminochrome (25 μM, for 48 h) induced morphological changes in the edge of slices and reduction of TH expression. These results demonstrate neuroinflammation, as well as negative regulation of neurotrophic factors (GDNF and NGF), may be involved in aminochrome-induced neurodegeneration, and they contribute to a better understanding of PD pathogenesis.

最近的证据表明，氨基色素可诱导与神经炎症相关的神经胶质活化。这种多巴胺衍生的分子可诱导α-突触核蛋白寡聚体的形成和稳定，线粒体功能障碍，氧化应激，蛋白酶体和溶酶体系统功能障碍，内质网应激和微管网络破坏，但直到现在，仍没有证据表明对多巴胺的产生有影响。细胞因子和神经营养因子，它们是帕金森氏病（PD）中神经元丢失的机制。这项研究探讨了氨基色素对P8-P9 Wistar大鼠器官型中脑切片培养物中NGF，GDNF，TNF-α和IL-1β产生以及小胶质细胞活化的调节的潜在作用。我们证明了氨基色素（25μM，持续24 h）诱导的GFAP表达降低，⁺细胞，并增加TNF-α，IL-1βmRNA和蛋白质水平。此外，氨基色素（25μM，持续48 h）诱导切片边缘的形态变化和TH表达降低。这些结果表明，神经炎症以及神经营养因子（GDNF和NGF）的负调控可能与氨基色素诱导的神经变性有关，它们有助于更好地了解PD的发病机理。