铜诱导的 M2 巨噬细胞极化在保护骨关节炎软骨基质中的作用

Dawei Geng, Rongcai Lin, Peiran Wei, Cheng Tang, Yan Xu, Liming Wang
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引用次数: 0

摘要

背景骨关节炎的病理机制尚不清楚。免疫微环境的调节在骨关节炎的进展和治疗中越来越受到关注。不同表型的巨噬细胞产生不同的细胞因子,这与骨关节炎软骨损伤的机制有关。铜离子在免疫反应中发挥作用,并通过影响软骨基质的新陈代谢参与骨关节炎的病理机制。生物活性玻璃(BG)是一种具有良好生物相容性的成骨材料。在此,我们报告了使用铜基复合 BG 材料对巨噬细胞的调控行为。材料与方法 采用溶胶-凝胶法制备了铜基 BGG 粉末,并使用 3D 打印技术制作了支架并对其进行了表征。对使用 Cu-BGC 培养的巨噬细胞进行了细胞培养和增殖检测。测定了 Cu-BGC 对在炎症细胞因子 IL-1ß 环境中培养的软骨细胞降解代谢的影响。此外,还考察了巨噬细胞的形态、炎症细胞因子的分泌和表面标志物的表达。结果 结果表明,在一定浓度范围内,Cu-BGC 可促进巨噬细胞增殖,增加抗炎细胞因子的分泌,同时抑制促炎细胞因子。同时,M2 型细胞表面标志物肯定会表达,巨噬细胞的形态也会发生改变。此外,Cu-BGC 还能抑制 IL-1ß 诱导的炎症环境中软骨细胞的降解代谢。结论 这些结果表明,Cu-BGC 可诱导巨噬细胞极化为 M2 型抗炎表型,抑制免疫损伤反应可能在延缓骨关节炎软骨基质损伤方面发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role of Copper-Induced M2 Macrophage Polarization in Protecting Cartilage Matrix in Osteoarthritis.
BACKGROUND The pathological mechanism of osteoarthritis is still unclear. The regulation of the immune microenvironment has been of growing interest in the progression and treatment of osteoarthritis. Macrophages with different phenotypes, producing different cytokines, have been linked to the mechanism of cartilage injury in osteoarthritis. Copper ions play a role in the immune response and are involved in the pathological mechanisms of osteoarthritis by affecting the metabolism of the cartilage matrix. Bioactive glass (BG) is an osteogenic material with superior biocompatibility. Here, we report on the regulatory behavior of macrophages using a copper-based composite BG material. MATERIAL AND METHODS Cu-BGC powder was prepared by sol-gel method, and scaffolds were fabricated and characterized using 3D printing. Macrophage cultures grown with Cu-BGC were examined for cell culture and proliferation. The effect of Cu-BGC on the degradation metabolism of chondrocytes, cultured in the environment of inflammatory cytokine IL-1ß, was determined. In addition, the morphology of macrophages, secretion of inflammatory cytokines, and expression of surface markers were examined. RESULTS The results show that Cu-BGC promotes macrophage proliferation at a range of concentrations and increases the secretion of anti-inflammatory cytokines while inhibiting proinflammatory cytokines. At the same time, M2-type cell surface markers are definitely expressed and the morphology of macrophages is altered. In addition, Cu-BGC inhibited the degradation metabolism of chondrocytes in the inflammatory environment induced by IL-1ß. CONCLUSIONS These results suggest that Cu-BGC induced macrophage polarization into an M2 type anti-inflammatory phenotype, and inhibition of immune injury response may play a role in delaying cartilage matrix damage in osteoarthritis.
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