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首页> 外文期刊>Brain research >Melatonin regulates neuroinflammation ischemic stroke damage through interactions with microglia in reperfusion phase
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Melatonin regulates neuroinflammation ischemic stroke damage through interactions with microglia in reperfusion phase

机译：褪黑激素通过再灌注相中的微血管相互作用来调节神经炎性缺血性脑卒中损伤

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摘要

Even today, ischemic stroke is a major cause of death and disabilities because of its high incidence, limited treatments and poor understanding of the pathophysiology of ischemia/reperfusion, neuroinflammation and secondary injuries following ischemic stroke. The function of microglia as a part of the immune system of the brain following ischemic stroke can be destructive or protective. Recent surveys indicate that melatonin, a strong antioxidant agent, has receptors on microglial cells and can regulate them to protective form; yet, more findings are required for better understanding of this mechanism, particularly in the reperfusion phase. In this study, we initially aimed to evaluate the therapeutic efficacy of melatonin intra-arterially and to clarify the underlying mechanisms. After that by using an in vitro approach, we evaluated the protective effects of melatonin on microglial cells following the hypoxia condition. Our results proved that a single dose of melatonin at the beginning of reperfusion phase improved structural and behavioral outcomes. Melatonin increased NeuN and decreased GFAP, Iba1 and active caspase-3 at protein level. Furthermore, melatonin elevated BDNF, MAP2, HSPA1A and reduced VEGF at mRNA level. We also showed that melatonin receptor 1B highly expressed in microglial cells after 3 h hypoxia. Besides, melatonin increased the ratio of TREM2/iNOS as a marker of the most protective form of microglia (M2). In summary, our data suggest that melatonin has the possibility to serve as targeting microglial action for preventing secondary injury of reperfusion phase after ischemic stroke.
机译：即使在今天，缺血性卒中也是死亡和残疾的主要原因，因为它具有高发病率，有限的治疗和对缺血性卒中后缺血性，神经炎，神经炎症和继发性损伤的病理生理学的理解。微胶质细胞作为脑卒中缺血性卒中后的免疫系统的一部分的功能可以是破坏性的或保护性的。最近的调查表明，褪黑激素是一种强抗氧化剂，具有小胶质细胞的受体，可以调节它们以保护形式;然而，更好地理解这种机制，特别是在再灌注阶段中，需要更多发现。在这项研究中，我们最初旨在评估褪黑激素内动脉内的治疗效果，并阐明潜在的机制。之后通过使用一种体外方法，我们评估了褪黑素对缺氧条件后微胶质细胞对微胶质细胞的保护作用。我们的结果证明，再灌注阶段开始的单剂量褪黑激素改善了结构和行为结果。褪黑激素在蛋白质水平上增加了Neun和降低的GFAP，IBA1和活性Caspase-3。此外，褪黑素升高的BDNF，MAP2，HSPA1A和MRNA水平的VEGF。我们还表明，在3小时缺氧后，褪黑激素受体1B在显微胶质细胞中高表达。此外，褪黑激素增加了Trem2 / InOS的比例作为MICROGLIA（M2）最具保护形式的标记物。总之，我们的数据表明褪黑激素可以作为靶向微胶质作用的可能性，以防止缺血性卒中后再灌注阶段的二次损伤。

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