IL-17A促进慢性痛风性关节炎中破骨细胞形成

doi:10.16352/j.issn.1001-6325.2025.12.1608

基础医学与临床 ›› 2025, Vol. 45 ›› Issue (12): 1608-1613.doi: 10.16352/j.issn.1001-6325.2025.12.1608

IL-17A促进慢性痛风性关节炎中破骨细胞形成

王一博, 狄虹, 张小涵, 张昀^*, 曾学军^*

中国医学科学院北京协和医学院北京协和医院全科医学科(普通内科),北京 100730

收稿日期:2025-07-25 修回日期:2025-09-15 出版日期:2025-12-05 发布日期:2025-11-25
通讯作者: ^*zhangyun10806@pumch.cn; zxjpumch@126.com
基金资助:
协和人才培育支持计划C类项目(UBJ10806);中央高水平医院临床科研专项(2022-PUMCH-B-044)

Interleukin-17A promotes osteoclastogenesis in chronic gouty arthritis

WANG Yibo, DI Hong, ZHANG Xiaohan, ZHANG Yun^*, ZENG Xuejun^*

Department of General Internal Medicine, Peking Union Medical College Hospital, PUMC & CAMS, Beijing 100730, China

Received:2025-07-25 Revised:2025-09-15 Online:2025-12-05 Published:2025-11-25
Contact: ^*zhangyun10806@pumch.cn; zxjpumch@126.com

摘要/Abstract

摘要： 目的慢性痛风性关节炎(CGA)患者存在严重骨破坏而导致关节畸形使得预后及生活质量不佳。CGA骨破坏主要由破骨细胞介导,课题组前期发现痛风关节局部IL-17A水平升高。本研究试图探究白细胞介素17A(IL-17A)对CGA患者骨破坏的影响及可能的作用机制。方法以健康对照和CGA患者外周血单个核细胞(PBMC)在体外诱导的破骨细胞为研究对象,CGA患者来源破骨细胞分为未处理组、IL-17A处理组、线粒体自噬激动剂羰基氰化物间氯苯腙(CCCP)处理组和线粒体分裂抑制剂1(Mdivi-1)处理组。采用抗酒石酸酸性磷酸酶染色法观察并比较健康对照和未处理组破骨细胞形成情况,利用Western blot检测线粒体自噬水平及破骨细胞关键分化因子的表达。结果与健康对照相比,CGA患者PBMC形成的破骨细胞数量更多(P＜0.01)。与未处理组相比,IL-17A组破骨细胞关键转录因子表达上调,线粒体自噬水平下降(P＜0.05)。10 nmol/L及15 nmol/L Mdivi-1的干预能够促进破骨细胞关键转录因子的表达(P＜0.01)。结论 IL-17A可促进CGA患者体外破骨细胞的形成,其作用机制可能和线粒体自噬水平下降有关。

关键词: 痛风, IL-17A, 破骨细胞, 线粒体自噬, 骨破坏

Abstract: Objective Chronic gouty arthritis (CGA) can lead to severe bone erosion resulting in joint destruction, which significantly decreases the life quality and prognosis of CGA patients. Osteoclasts play an important role in this course. We aim to investigate the effect of interleukin-17A (IL-17A) on osteoclast formation in vitro in patients with chronic gouty arthritis (CGA) and its potential mechanism. Methods Osteoclasts induced in vitro from peripheral blood mononuclear cells (PBMC) of healthy controls (HC) and CGA patients were studied. CGA-derived osteoclasts were divided into four groups: untreated group, IL-17A-treated group, carbonyl cyanide 3-chlorophenylhydrazone (CCCP) group, and mitochondrial division inhibitor-1 (Mdivi-1) group. Tartrate-resistant acid phosphatase (TRAP) staining was used to observe and compare osteoclastogenesis between HC and the untreated group. Western blot was performed to detect mitophagy levels and the expression of key osteoclast differentiation factors. Results Compared with healthy controls, CGA patients showed higher osteoclastogenesis(P＜0.01). Compared with the untreated group, the IL-17A-treated group showed up-regulated expression of key osteoclast transcription factors and decreased mitophagy levels (P＜0.05). Intervention with 10 nmol/L and 15 nmol/L Mdivi-1 significantly promoted the expression of key osteoclast transcription factors (P＜0.01). Conclusions IL-17A promotes osteoclast formation in vitro in CGA patients, and its mechanism may be related to decreased mitophagy levels.

Key words: gout, IL-17A, osteoclast, mitophagy, bone erosion

中图分类号:

R593.9

王一博, 狄虹, 张小涵, 张昀, 曾学军. IL-17A促进慢性痛风性关节炎中破骨细胞形成[J]. 基础医学与临床, 2025, 45(12): 1608-1613.

WANG Yibo, DI Hong, ZHANG Xiaohan, ZHANG Yun, ZENG Xuejun. Interleukin-17A promotes osteoclastogenesis in chronic gouty arthritis[J]. Basic & Clinical Medicine, 2025, 45(12): 1608-1613.

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IL-17A促进慢性痛风性关节炎中破骨细胞形成

Interleukin-17A promotes osteoclastogenesis in chronic gouty arthritis

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