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.