CXCL13/CXCR5 promote chronic postsurgical pain and astrocyte activation in rats by targeting NLRP3.

IF 1.6 4区 医学 Q4 NEUROSCIENCES Neuroreport Pub Date : 2024-04-03 Epub Date: 2024-03-07 DOI:10.1097/WNR.0000000000002023
Hongda Yi, Bin Zhu, Caihong Zheng, Zhenyang Ying, Mei Cheng
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Abstract

Chronic postsurgical pain (CPSP) with high incidence negatively impacts the quality of life. X-C motif chemokine 13 (CXCL13) has been associated with postsurgery inflammation and exacerbates neuropathic pain in patients with CPSP. This study was aimed to illustrate the relationship between CXCL13 and nod-like receptor protein-3 (NLRP3), which is also involved in CPSP. A CPSP model was constructed by skin/muscle incision and retraction (SMIR) in right medial thigh, and the rats were divided into three groups: Sham, SMIR, and SMIR + anti-CXCL13 (intrathecally injected with anti-CXCL13 antibody). Then, the paw withdrawal threshold (PWT) score of rats was recorded. Primary rat astrocytes were isolated and treated with recombinant protein CXCL13 with or without NLRP3 inhibitor INF39. The expressions of CXCL13, CXCR5, IL-1β, IL-18, GFAP, NLRP3, and Caspase-1 p20 were detected by real-time quantitative reverse transcription PCR, western blot, ELISA, immunocytochemistry, and immunofluorescence analyses. The anti-CXCL13 antibody alleviated SMIR-induced decreased PWT and increased expression of GFAP, CXCL13, CXCR5, NLRP3, and Caspase-1 p20 in spinal cord tissues. The production of IL-1β, IL-18, and expression of CXCL13, CXCR5, GFAP, NLRP3, and Caspase-1 p20 were increased in recombinant protein CXCL13-treated primary rat astrocytes in a dose-dependent manner. Treatment with NLRP3 inhibitor INF39 inhibited the function of recombinant protein CXCL13 in primary rat astrocytes. The CXCL13/CXCR5 signaling could promote neuropathic pain, astrocytes activation, and NLRP3 inflammasome activation in CPSP model rats by targeting NLRP3. NLRP3 may be a potential target for the management of CPSP.

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CXCL13/CXCR5 通过靶向 NLRP3 促进大鼠手术后慢性疼痛和星形胶质细胞活化。
慢性手术后疼痛(CPSP)发病率很高,对患者的生活质量造成了负面影响。X-C motif趋化因子13(CXCL13)与手术后炎症有关,会加剧CPSP患者的神经病理性疼痛。本研究旨在说明 CXCL13 与同样参与 CPSP 的类结节受体蛋白-3(NLRP3)之间的关系。通过右大腿内侧皮肤/肌肉切开和牵引(SMIR)建立了 CPSP 模型,并将大鼠分为三组:大鼠分为三组:Sham组、SMIR组和SMIR + anti-CXCL13 组(鞘内注射抗CXCL13抗体)。然后记录大鼠爪退缩阈值(PWT)评分。分离原代大鼠星形胶质细胞,并用重组蛋白 CXCL13 加或不加 NLRP3 抑制剂 INF39 处理。通过实时定量反转录 PCR、Western 印迹、ELISA、免疫细胞化学和免疫荧光分析检测了 CXCL13、CXCR5、IL-1β、IL-18、GFAP、NLRP3 和 Caspase-1 p20 的表达。抗CXCL13抗体缓解了SMIR诱导的脊髓PWT下降和脊髓组织中GFAP、CXCL13、CXCR5、NLRP3和Caspase-1 p20表达的增加。重组蛋白 CXCL13 处理的原代大鼠星形胶质细胞中,IL-1β、IL-18 的产生以及 CXCL13、CXCR5、GFAP、NLRP3 和 Caspase-1 p20 的表达均呈剂量依赖性增加。NLRP3 抑制剂 INF39 可抑制重组蛋白 CXCL13 在原代大鼠星形胶质细胞中的功能。通过靶向 NLRP3,CXCL13/CXCR5 信号传导可促进 CPSP 模型大鼠的神经病理性疼痛、星形胶质细胞活化和 NLRP3 炎性体活化。NLRP3可能是治疗CPSP的潜在靶点。
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来源期刊
Neuroreport
Neuroreport 医学-神经科学
CiteScore
3.20
自引率
0.00%
发文量
150
审稿时长
1 months
期刊介绍: NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
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