Kane Cynthia J M, Drew Paul D
Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
J Leukoc Biol. 2016 Nov;100(5):951-959. doi: 10.1189/jlb.3MR0416-171R. Epub 2016 Jul 26.
Fetal alcohol spectrum disorder (FASD), which results from ethanol exposure during pregnancy, and alcohol use disorder (AUD), which includes both binge and chronic alcohol abuse, are strikingly common and costly at personal and societal levels. These disorders are associated with significant pathology, including that observed in the CNS. It is now appreciated in both humans and animal models that ethanol can induce inflammation in the CNS. Neuroinflammation is hypothesized to contribute to the neuropathologic and behavioral consequences in FASD and AUD. In this review, we: 1) summarize the evidence of alcohol-induced CNS inflammation, 2) outline cellular and molecular mechanisms that may underlie alcohol induction of CNS inflammation, and 3) discuss the potential of nuclear receptor agonists for prevention or treatment of neuropathologies associated with FASD and AUD.
胎儿酒精谱系障碍(FASD)由孕期接触乙醇所致,而酒精使用障碍(AUD)包括暴饮和慢性酒精滥用,这两种病症在个人和社会层面都极为常见且代价高昂。这些病症与重大病理状况相关,包括中枢神经系统(CNS)中观察到的病理状况。目前在人类和动物模型中均已认识到,乙醇可在中枢神经系统中诱发炎症。神经炎症被认为是导致FASD和AUD中神经病理和行为后果的原因。在本综述中,我们:1)总结酒精诱发中枢神经系统炎症的证据,2)概述可能是酒精诱发中枢神经系统炎症基础的细胞和分子机制,3)讨论核受体激动剂在预防或治疗与FASD和AUD相关的神经病理方面的潜力。