代谢紊乱药物在小胶质细胞介导的神经炎症中缓解 CXCL10 的分泌

IF 2.9 4区 医学 Q3 IMMUNOLOGY
Sophia F. Oliai , Daniel C. Shippy , Tyler K. Ulland
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引用次数: 0

摘要

代谢紊乱与多种神经退行性疾病有关。我们之前发现 C-X-C motif 趋化因子配体 10 (CXCL10),又称γ干扰素诱导蛋白 10 (IP-10),是小胶质细胞介导的神经炎症中 I 型干扰素反应的主要促成因素。因此,我们假设美国食品与药物管理局批准的可减少 CXCL10 分泌的代谢紊乱药物可重新用于治疗神经退行性疾病。通过在 LPS 刺激的小胶质细胞中进行筛选、剂量曲线和细胞毒性试验,我们发现曲普瑞替尼尔(高血压)、匹伐他汀(高脂血症)和依普利酮(高血压)等候选药物能显著减少 CXCL10(以及其他促炎介质)的分泌,同时不影响细胞活力。总之,这些数据表明,通过减轻小胶质细胞介导的神经炎症,减轻 CXCL10 的代谢紊乱药物是治疗神经退行性疾病的潜在药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mitigation of CXCL10 secretion by metabolic disorder drugs in microglial-mediated neuroinflammation

Mitigation of CXCL10 secretion by metabolic disorder drugs in microglial-mediated neuroinflammation

Metabolic disorders are associated with several neurodegenerative diseases. We previously identified C-X-C motif chemokine ligand 10 (CXCL10), also known as interferon gamma-induced protein 10 (IP-10), as a major contributor to the type I interferon response in microglial-mediated neuroinflammation. Therefore, we hypothesized FDA-approved metabolic disorder drugs that attenuate CXCL10 secretion may be repurposed as a treatment for neurodegenerative diseases. Screening, dose curves, and cytotoxicity assays in LPS-stimulated microglia yielded treprostinil (hypertension), pitavastatin (hyperlipidemia), and eplerenone (hypertension) as candidates that significantly reduced CXCL10 secretion (in addition to other pro-inflammatory mediators) without impacting cell viability. Altogether, these data suggest metabolic disorder drugs that attenuate CXCL10 as potential treatments for neurodegenerative disease through mitigating microglial-mediated neuroinflammation.

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来源期刊
Journal of neuroimmunology
Journal of neuroimmunology 医学-免疫学
CiteScore
6.10
自引率
3.00%
发文量
154
审稿时长
37 days
期刊介绍: The Journal of Neuroimmunology affords a forum for the publication of works applying immunologic methodology to the furtherance of the neurological sciences. Studies on all branches of the neurosciences, particularly fundamental and applied neurobiology, neurology, neuropathology, neurochemistry, neurovirology, neuroendocrinology, neuromuscular research, neuropharmacology and psychology, which involve either immunologic methodology (e.g. immunocytochemistry) or fundamental immunology (e.g. antibody and lymphocyte assays), are considered for publication.
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