营养或药理学激活 HCA(2)可改善神经炎症。
Nutritional or pharmacological activation of HCA(2) ameliorates neuroinflammation.
机构信息
Department of Pharmacology, Max Planck Institute for Heart and Lung Research, Ludwigstrasse 43, 61231 Bad Nauheim, Germany; Medical Faculty, J.W. Goethe University, Frankfurt, Germany.
Institute of Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany; DZHK (German Research Centre for Cardiovascular Research), partner site Hamburg/Lübeck/Kiel, 23562 Lübeck, Germany.
出版信息
Trends Mol Med. 2015 Apr;21(4):245-55. doi: 10.1016/j.molmed.2015.02.002. Epub 2015 Mar 9.
Neuroinflammation is a pathology common to many neurological diseases, including multiple sclerosis (MS) and stroke. However, therapeutic attempts to modulate neuroinflammation have proved difficult. Neuroinflammatory cells express HCA2, a receptor for the endogenous neuroprotective ketone body β-hydroxybutyrate (BHB) as well as for the drugs dimethyl fumarate (DMF) and nicotinic acid, which have established efficacy in the treatment of MS and experimental stroke, respectively. This review summarizes the evidence that HCA2 is involved in the therapeutic effects of DMF, nicotinic acid, and ketone bodies in reducing neuroinflammation. Furthermore, we discuss the mechanisms underlying the beneficial effects of HCA2 activation in neuroinflammatory diseases and the therapeutic potential of recently developed synthetic ligands of HCA2.
神经炎症是许多神经疾病共有的病理学，包括多发性硬化症 (MS) 和中风。然而，调节神经炎症的治疗尝试证明是困难的。神经炎症细胞表达 HCA2，这是内源性神经保护酮体β-羟基丁酸 (BHB) 的受体，也是药物二甲基富马酸 (DMF) 和烟酸的受体，它们在治疗 MS 和实验性中风方面分别具有疗效。这篇综述总结了 HCA2 参与 DMF、烟酸和酮体治疗神经炎症的证据，这些物质可以减轻神经炎症。此外，我们还讨论了 HCA2 激活在神经炎症性疾病中的有益作用的潜在机制，以及最近开发的 HCA2 合成配体的治疗潜力。
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