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| NF-κB调控巨噬细胞极化在骨性关节炎中作用的研究进展 |
| Research Progress on the Role of NF-κB-Regulated Macrophage Polarization in Osteoarthritis |
| 投稿时间：2025-10-21 修订日期：2026-04-03 |
| DOI： |
| 中文关键词: NF-κB信号通路 巨噬细胞极化 骨性关节炎 |
| 英文关键词:NF-κB Signaling Pathway Macrophage Polarization Osteoarthritis |
| 基金项目:益肾健骨丸对大鼠膝骨性关节炎软骨细胞的凋亡影响的实验研究；益肾健骨丸通过STAT3-HSP70-PRKACB轴调控糖酵解代谢及巨噬细胞极化改善膝骨关节炎炎症反应的机制研究 |
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| 中文摘要: |
| 骨性关节炎（Osteoarthritis, OA）作为一种退行性疾病，其发病是多种因素共同作用的结果，这些因素导致关节软骨出现纤维化、皲裂、溃疡及脱失等病理改变，临床上主要表现为关节疼痛，目前其确切病因尚未明确。该疾病的病理进程以关节局部炎症失衡为核心病理机制。核因子-κB（nuclear factor-kappa B, NF-κB）信号通路是调控OA炎症的关键枢纽，其过度激活会双向调控巨噬细胞极化：一方面驱动巨噬细胞向M1型极化，通过分泌促炎因子，结合共刺激分子激活T细胞、募集炎性细胞，形成OA滑膜炎症恶循环，加重关节组织损伤；另一方面抑制巨噬细胞向M2型极化，通过竞争转录位点、干扰代谢等方式，减少抗炎因子释放，最终削弱OA关节组织的自我修复能力，推动OA从早期软骨退变向中晚期关节畸形、功能障碍的病理进展。本文综述了NF-κB调控巨噬细胞极化在OA中的作用机制，明确了NF-κB—巨噬细胞极化轴。并阐述天然产物、纳米载体、细胞因子三大干预策略对NF-κB—巨噬细胞极化轴的调控效果，旨在为该疾病的靶向治疗提供理论依据。 |
| 英文摘要: |
| Osteoarthritis (OA), a degenerative joint disorder, arises from the synergistic action of multiple etiological factors. These factors induce a series of pathological changes in articular cartilage, including fibrosis, fissuring, ulceration and erosion. Clinically, OA is primarily characterized by joint pain, while its exact pathogenesis remains elusive to date. The core pathological mechanism underlying the progression of OA is the dysregulation of local joint inflammation. The nuclear factor-kappa B (NF-κB) signaling pathway serves as a key hub governing OA-associated inflammation, and its aberrant overactivation exerts a bidirectional regulatory effect on macrophage polarization. On the one hand, it drives the polarization of macrophages toward the pro-inflammatory M1 phenotype. Polarized M1 macrophages secrete pro-inflammatory cytokines and interact with co-stimulatory molecules to activate T cells and recruit inflammatory cells, thereby forming a vicious cycle of synovial inflammation in OA and exacerbating joint tissue damage. On the other hand, hyperactivated NF-κB signaling inhibits macrophage polarization toward the anti-inflammatory M2 phenotype via mechanisms such as competitive binding to transcription sites and metabolic interference. This suppression reduces the secretion of anti-inflammatory cytokines, ultimately impairing the self-repair capacity of OA joint tissues and facilitating the pathological progression of OA from early-stage cartilage degeneration to middle- and late-stage joint deformity and dysfunction. This review summarizes the regulatory mechanisms of NF-κB-mediated macrophage polarization in OA and clarifies the NF-κB-macrophage polarization axis. Furthermore, it elaborates on the regulatory effects of three major intervention strategies, namely natural products, nanocarriers and cytokines, on this axis, aiming to provide a theoretical basis for the targeted therapy of OA. |
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