芒果苷通过抑制巨噬细胞NF-κB调节巨噬细胞极化为M2，探索芒果苷治疗骨关节炎的潜在机制。

RAW264.7小鼠巨噬细胞系进行体外培养，IL-4诱导巨噬细胞M₂极化，用芒果苷对巨噬细胞进行干预。实验分为空白组、对照组和实验组。CCK-8检测芒果苷的细胞毒性。钙黄绿素（Calcein-AM）和碘化丙啶（PI）双荧光染色法检测细胞活性，流式细胞仪检测细胞凋亡的情况。免疫荧光染色评估甘露糖受体（CD206抗体）在巨噬细胞的分泌情况，实时荧光定量PCR（qRT-PCR）法检测NF-κB通路相关基因RelA（p65）及M2巨噬细胞相关基因CD206、IL-10的表达情况。

浓度为20 μM的芒果苷对巨噬细胞无明显毒性作用，芒果苷在该浓度下能显著下调RelA的表达和上调IL-10、CD206的表达，从而抑制NF-κB通路激活巨噬细胞M2极化。

芒果苷能够抑制巨噬细胞NF-κB调节巨噬细胞极化为M2，M2巨噬细胞具有抗炎功能，促进软骨修复功能，为芒果苷在骨关节炎的研究中提供可能的机制理论。

To investigate the effect of mangiferin on the treatment of osteoarthritis by inhibiting the NF-κB pathway and regulating the polarization of macrophages to M2.

The RAW264.7 mouse macrophage cell line was cultured in vitro, IL-4 induced M2 polarization of macrophages, and the macrophages were intervened with mangiferin. The experiment was divided into blank group, control group and experimental group. CCK-8 detected the cytotoxicity of mangiferin. Calcein-AM (calcein) and PI (propidium iodide) double fluorescent staining was used to detect cell viability, and flow cytometry was used to detect cell apoptosis. Immunofluorescence staining was used to evaluate the secretion of mannose receptor (CD206 antibody) in macrophages, and real-time quantitative PCR (qRT-PCR) was used to detect the NF-κB pathway-related gene RelA (p65) and M2 macrophage-related genes CD206, IL-10 expression.

Mangiferin at a concentration of 20 μM had no significant toxic effect on macrophages, and mangiferin could significantly down-regulate the expression of RelA and up-regulate the expression of 1L-10 and CD206 at this concentration, thereby inhibiting the activation of M2 macrophages by the NF-κB pathway and thus alleviating arthritis in mice.

Mangiferin can inhibit the NF-κB pathway and regulate the polarization of macrophages to M2. M2 macrophages have anti-inflammatory functions and promote cartilage repair, which may provide a theoretical basis for new treatment of osteoarthritis.