Department of Propedeutics of Neurology, Medical University of Lodz, ul. Pabianicka 62, Lodz, Poland.
Mediators Inflamm. 2013;2013:727189. doi: 10.1155/2013/727189. Epub 2013 Nov 11.
Neurodegeneration is a hallmark of most of the central nervous system (CNS) disorders including stroke. Recently inflammation has been implicated in pathogenesis of neurodegeneration and neurodegenerative diseases. The aim of this study was analysis of expression of several inflammatory markers and its correlation with development of neurodegeneration during the early stage of experimental stroke. Ischemic stroke model was induced by stereotaxic intracerebral injection of vasoconstricting agent endothelin-1 (ET-1). It was observed that neurodegeneration appears very early in that model and correlates well with migration of inflammatory lymphocytes and macrophages to the brain. Although the expression of several studied chemotactic cytokines (chemokines) was significantly increased at the early phase of ET-1 induced stroke model, no clear correlation of this expression with neurodegeneration was observed. These data may indicate that chemokines do not induce neurodegeneration directly. Upregulated in the ischemic brain chemokines may be a potential target for future therapies reducing inflammatory cell migration to the brain in early stroke. Inhibition of inflammatory cell accumulation in the brain at the early stage of stroke may lead to amelioration of ischemic neurodegeneration.
神经退行性变是大多数中枢神经系统（CNS）疾病的标志，包括中风。最近，炎症被认为与神经退行性变和神经退行性疾病的发病机制有关。本研究的目的是分析几种炎症标志物的表达及其与实验性中风早期神经退行性变的发展的相关性。通过立体定向脑内注射血管收缩剂内皮素-1（ET-1）诱导缺血性中风模型。结果表明，在该模型中神经退行性变出现得非常早，并且与炎症性淋巴细胞和巨噬细胞向大脑的迁移密切相关。尽管在 ET-1 诱导的中风模型的早期阶段几种研究趋化因子（趋化因子）的表达显著增加，但没有观察到这种表达与神经退行性变之间的明显相关性。这些数据可能表明趋化因子不会直接引起神经退行性变。在缺血性大脑中上调的趋化因子可能是未来治疗的潜在靶点，可减少中风早期炎症细胞向大脑的迁移。在中风的早期阶段抑制炎症细胞在大脑中的积累可能会改善缺血性神经退行性变。
