UNASSIGNED:研究静磁场(SMF)在骨关节炎软骨修复中的治疗作用及其调节机制。
UNASSIGNED: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,有无SMF应用。SMF以200mT连续两周施用。通过组织形态学检查膝关节软骨的变化,并对内源性干细胞的软骨形成和迁移进行了评估。SRY相关蛋白9(SOX9)的表达,II型胶原(COL2),基质金属肽酶13(MMP13),基质细胞衍生因子1/C-X-C趋化因子受体4(SDF-1/CXCR4),Piezo1和其他基因进行了评估,并使用CXCR4抑制剂测试SMF的作用机制,AMD3100和Piezo1siRNA。
UNASSIGNED:SMF在诱导OA后显著降低OARSI评分。SMF通过升高SOX9有利于软骨形成。在OA小鼠模型中,随着COL2的减少,MMP13的增加导致软骨细胞外基质的破坏,被SMF压制。SMF促进软骨来源的干/祖细胞和骨髓来源的间充质干细胞(MSCs)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。Piezo1siRNA的应用抑制了SMF诱导的CXCR4的增加。
UNASSIGNED:SMF增强了软骨形成并改善了软骨细胞外基质。它激活Piezo1介导的SDF-1/CXCR4调节轴,促进内源性干细胞的迁移。总的来说,它减轻了OA小鼠软骨破坏的病理进展。
UNASSIGNED:这项研究的发现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,提示SMF在OA治疗中具有临床价值。
UNASSIGNED: To investigate the therapeutic effects of static magnetic field (SMF) and its regulatory mechanism in the repair of osteoarthritic cartilage.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.