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乌帕达西替尼 (Upadacitinib) 调节与疼痛相关的途径和BDNF表达在人类单细胞衍生的微质状细胞中

M Vomero¹, E Corberi², O Berardicurti³

¹Clinical unit of Immunorheumatology, Fondazione Policlinico Universitario Campus Bio-Medico, Via Alvaro del Portillo, 200, 00128 Roma, Italy; Department of Sciences and Technologies for Sustainable Development and One Health, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo, 21, 00128 Rome, Italy.

Brain, behavior, and immunity

|July 13, 2025

概括

乌帕丁尼 (upa) 是一种JAK1抑制剂,通过降低微状细胞中的脑衍生神经营养因子 (BDNF) 的调节来减少疼痛. 这种治疗促进了抗nociceptive的形状,缓解慢性疼痛在炎症条件下.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

慢性疼痛在炎症性关节炎中持续存在,尽管关节炎症减少.
微质细胞通过IL-1β和BDNF等细胞因子促进神经炎症和疼痛.
一种JAK1抑制剂Upadacitinib (upa) 在减少疾病活性和疼痛方面表现出有效性,但其缓解疼痛的机制需要澄清.

研究的目的:

研究如何UPA影响疼痛和神经炎症相关的分子在人类微状细胞模型.
具体来说,要确定upa对BDNF生产及其潜在机制的影响.

主要方法:

使用一种亲炎性人类单细胞衍生微状细胞 (M1-MDMi) 细胞模型.
在体外应用上达西替尼 (upa) 治疗以抑制JAK1.1.
进行了转录组分析,以评估基因表达变化.

主要成果:

在Upadacitinib治疗下调了BDNF的表达和分泌.
这种下调是通过P2X4受体的调节来调节的.
转录组分析显示,UPA通过减少神经炎症和与疼痛相关的途径来诱导一种抗 nociceptive 配置.

结论:

由upadacitinib抑制JAK1有效地降低了微状细胞中BDNF的产生.
乌帕达西替尼调节P2X4受体,影响中心疼痛感知机制.
乌帕达西尼布通过促进抗nociceptive状态,显示出作为慢性疼痛治疗剂的潜力.

关键词:

这就是为什么BDNF是BDNF.质细胞是质细胞的组成部分.抑制了JAK1的发生.神经炎症是一种神经炎症.这是一个P2X4RR.疼痛疼痛疼痛疼痛

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