Cordaro Marika, Cuzzocrea Salvatore, Crupi Rosalia
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Via Consolare Valeria 1, 98100 Messina, Italy.
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Via F. Stagno D'Alcontres 31, 98166 Messina, Italy.
Antioxidants (Basel). 2020 Mar 5;9(3):216. doi: 10.3390/antiox9030216.
The inflammation process represents of a dynamic series of phenomena that manifest themselves with an intense vascular reaction. Neuroinflammation is a reply from the central nervous system (CNS) and the peripheral nervous system (PNS) to a changed homeostasis. There are two cell systems that mediate this process: the glia of the CNS and the lymphocites, monocytes, and macrophages of the hematopoietic system. In both the peripheral and central nervous systems, neuroinflammation plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson's and Alzheimer's diseases, and in neuropsychiatric illnesses, such as depression and autism spectrum disorders. The resolution of neuroinflammation is a process that allows for inflamed tissues to return to homeostasis. In this process the important players are represented by lipid mediators. Among the naturally occurring lipid signaling molecules, a prominent role is played by the N-acylethanolamines, namely N-arachidonoylethanolamine and its congener N-palmitoylethanolamine, which is also named palmitoylethanolamide or PEA. PEA possesses a powerful neuroprotective and anti-inflammatory power but has no antioxidant effects per se. For this reason, its co-ultramicronization with the flavonoid luteolin is more efficacious than either molecule alone. Inhibiting or modulating the enzymatic breakdown of PEA represents a complementary therapeutic approach to treating neuroinflammation. The aim of this review is to discuss the role of ultramicronized PEA and co-ultramicronized PEA with luteolin in several neurological diseases using preclinical and clinical approaches.
炎症过程是一系列动态现象的表现，伴随着强烈的血管反应。神经炎症是中枢神经系统（CNS）和外周神经系统（PNS）对体内稳态变化的一种反应。有两个细胞系统介导这一过程：中枢神经系统的神经胶质细胞以及造血系统的淋巴细胞、单核细胞和巨噬细胞。在周围神经系统和中枢神经系统中，神经炎症在神经退行性疾病（如帕金森病和阿尔茨海默病）以及神经精神疾病（如抑郁症和自闭症谱系障碍）的发病机制中都起着重要作用。神经炎症的消退是一个使炎症组织恢复体内稳态的过程。在这个过程中，脂质介质起着重要作用。在天然存在的脂质信号分子中，N-酰基乙醇胺发挥着突出作用，即N-花生四烯酰乙醇胺及其同系物N-棕榈酰乙醇胺，后者也被称为棕榈酰乙醇胺或PEA。PEA具有强大的神经保护和抗炎能力，但本身没有抗氧化作用。因此，它与类黄酮木犀草素的共超微细化比单独使用任何一种分子都更有效。抑制或调节PEA的酶促分解是治疗神经炎症的一种补充治疗方法。本综述的目的是使用临床前和临床方法，探讨超微细化PEA以及PEA与木犀草素共超微细化在几种神经系统疾病中的作用。
