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

The role of NF-κB (p65) in Glaucocalyxin B-induced inhibition of SMG M1 polarization. (A–B) P65 silencing could inhibit SMG M1 polarization and Gla B cannot further inhibit M1 polarization. There was no difference between groups. Comparison with L/I, *P C–I) Detection of M1/M2 cell marker proteins. Gla B cannot further down-regulate the levels of TNF-α, IL-1β, IL-6, iNOS and IL-12 in P65 silenced cells. Comparison with L/I, *P J) Detection of ROS showed that Gla B could not further down-regulate the level of ROS in cells with P65 silencing.

Figure 3. The role of NF-κB (p65) in Glaucocalyxin B-induced inhibition of SMG M1 polarization. (AB) P65 silencing could inhibit SMG M1 polarization and Gla B cannot further inhibit M1 polarization. There was no difference between groups. Comparison with L/I, *P < 0.05. (CI) Detection of M1/M2 cell marker proteins. Gla B cannot further down-regulate the levels of TNF-α, IL-1β, IL-6, iNOS and IL-12 in P65 silenced cells. Comparison with L/I, *P < 0.05. (J) Detection of ROS showed that Gla B could not further down-regulate the level of ROS in cells with P65 silencing.