脑啡肽治疗改善复发-缓解型多发性硬化症

Chirag Patel, I. Zagon, G. Thomas, P. McLaughlin
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引用次数: 4

摘要

多发性硬化症(MS)伴随着血清内源性脑啡肽/内啡肽的减少和炎症细胞因子的改变。这项血清水平的回顾性分析是在53例已确定的复发缓解型MS患者中进行的,这些患者接受了疾病修饰疗法(DMT)醋酸格拉替默、富马酸二甲酯或生物治疗性低剂量纳曲酮(LDN)来提高脑啡肽水平,这是一种标签外替代疗法。测定阿片生长因子(OGF)与血清β-内啡肽、IL-17A和TNFα的相关性,OGF是一种抑制细胞复制的内源性阿片。结果显示,MS导致DMTs受试者的OGF水平显著降低,但LDN患者的OGF水平与非MS对照组相当。服用DMTs的患者TNFα水平显著升高,而IL-17A水平仅在服用富马酸二甲酯的患者中显著升高。在OGF和IL17A之间建立了直接相关性,表明OGF- ogfr轴和促炎t辅助细胞之间存在潜在的相互作用,为了解疾病的病因提供了线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Enkephalin Therapy Improves Relapsing-Remitting Multiple Sclerosis
Multiple sclerosis (MS) is accompanied by decreases in serum endogenous enkephalin/endorphins and alterations in inflammatory cytokines. This retrospective analysis of serum levels was conducted in 53 patients with established relapsing-remitting MS treated with the disease-modifying therapies (DMT) glatiramer acetate, dimethyl fumarate or with the biotherapeutic low dose naltrexone (LDN) to elevate enkephalins, an off-label alternative. Opioid growth factor (OGF), an inhibitory endogenous opioid involved in modulating cellular replication, was measured and correlated to serum β-endorphin, IL-17A and TNFα. Results revealed that MS leads to a significant reduction in OGF levels in subjects on DMTs, but patients on LDN had OGF levels comparable to non-MS controls. Individuals on DMTs had significantly elevated TNFα levels, while IL-17A levels were significantly elevated only in patients taking dimethyl fumarate. A direct correlation was established between OGF and IL17A indicating a potential interaction between the OGF-OGFr axis and pro-inflammatory T-helper cells providing insight into the disease etiology.
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