静磁场通过促进干细胞的迁移和软骨形成来增强骨关节炎软骨的修复,Journal of Orthopaedic Translation

探讨静磁场（SMF）在骨关节炎软骨修复中的治疗作用及其调控机制。

将 14 周龄雌性 C57BL/6 小鼠随机分为假手术组和骨关节炎 (OA) 组，使用和不使用 SMF。连续两周以 200 mT 施加 SMF。通过组织形态学检查膝关节软骨的变化，并评估内源性干细胞的软骨形成和迁移。SRY相关蛋白9（SOX9）、II型胶原蛋白（COL2）、基质金属肽酶13（MMP13）、基质细胞衍生因子1/CXC趋化因子受体4型（SDF-1/CXCR4）、Piezo1等基因的表达进行了评估，并使用 CXCR4 抑制剂、AMD3100 和 Piezo1 siRNA 测试了 SMF 的作用机制。

SMF 显着降低了 OA 诱导后的 OARSI 评分。SMF 通过升高 SOX9 有利于软骨形成。在 OA 小鼠模型中，MMP13 的增加和 COL2 的减少导致软骨细胞外基质的破坏，这被 SMF 抑制。SMF 促进软骨来源的干/祖细胞和骨髓来源的间充质干细胞 (MSC) 的迁移。它增加了 SDF-1 和 CXCR4，而 CXCR4 抑制剂显着抑制了 SMF 的有益作用。Piezo1 siRNA 的应用抑制了 SMF 诱导的 CXCR4 增加。

SMF 增强软骨形成并改善软骨细胞外基质。它激活了 Piezo1 介导的 SDF-1/CXCR4 调节轴并促进了内源性干细胞的迁移。总的来说，它减弱了 OA 小鼠软骨破坏的病理进展。

本研究的结果提供了令人信服的证据，表明 SMF 可以增强软骨修复并改善 OA 症状，表明 SMF 在治疗 OA 方面具有临床价值。

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Objective

To investigate the therapeutic effects of static magnetic field (SMF) and its regulatory mechanism in the repair of osteoarthritic cartilage.

Fourteen-week-old female C57BL/6 mice were randomly divided into the sham operation group and the osteoarthritis (OA) groups with and without SMF application. SMF was applied at 200 ​mT for two consecutive weeks. Changes in knee cartilage were examined by histomorphometry, and the chondrogenesis and migration of endogenous stem cells were assessed. The expression of SRY-related protein 9 (SOX9), Collagen type II (COL2), matrix metallopeptidase 13 (MMP13), stromal cell-derived factor 1/C-X-C chemokine receptor type 4 (SDF-1/CXCR4), Piezo1 and other genes was evaluated, and the mechanism of SMF's action was tested using the CXCR4 inhibitor, AMD3100, and Piezo1 siRNA.

SMF significantly decreased the OARSI scores after induction of OA. SMF was beneficial to chondrogenesis by elevating SOX9. In the OA mouse model, an increase in MMP13 with a decrease in COL2 led to the destruction of the cartilage extracellular matrix, which was suppressed by SMF. SMF promoted the migration of cartilage-derived stem/progenitor cells and bone marrow-derived mesenchymal stem cells (MSCs). It increased SDF-1 and CXCR4, while the CXCR4 inhibitor significantly suppressed the beneficial effects of SMF. The application of Piezo1 siRNA inhibited the SMF-induced increase of CXCR4.

SMF enhanced chondrogenesis and improved cartilage extracellular matrices. It activated the Piezo1-mediated SDF-1/CXCR4 regulatory axis and promoted the migration of endogenous stem cells. Collectively, it attenuated the pathological progression of cartilage destruction in OA mice.

The findings in this study provided convincing evidence that SMF could enhance cartilage repair and improve OA symptoms, suggesting that SMF could have clinical value in the treatment of OA.