Research Paper Volume 13, Issue 18 pp 22544—22555

Glaucocalyxin B inhibits cartilage inflammatory injury in rheumatoid arthritis by regulating M1 polarization of synovial macrophages through NF-κB pathway

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Figure 1. The effect of Gla B on SMG M1 polarization. (AB) Detection of the ratio of F4/80+CD86+ M1 type cells by flow cytometry. LPS/IFN-γ could promote SMG M1 type polarization. Gla B could inhibit polarization and decrease the ratio of F4/80+CD86+ cells. Comparison with DMSO, *P < 0.05; comparison with L/I, #P < 0.05. (CF) and (I) Detection of M1 type cell marker. After LPS and IFN-γ treatment to induce M1 polarization, the levels of TNF-α, IL-1β, IL-6, iNOS and IL-12 were significantly up-regulated, and Gla B could inhibit the up-regulation of cytokines. Comparison with DMSO, *P < 0.05; comparison with L/I, #P < 0.05. (GH) Detection of M2 type cell marker. After LPS and IFN-γ treatment to induce M1 polarization, the expression of TGF-β1 and IL-10 was not significantly changed, while Gla B also had no effect on the expression of TGF-β1 and IL-10. nsP < 0.05. (J) Detection of ROS by DCFH-DA. After LPS and IFN-γ treatment to induce M1 polarization, the expression of ROS was significantly up-regulated while Gla B inhibited the expression of ROS.