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

M1-SMG induced cartilage cell injury. (A–B) The results of flow cytometry showed that SMG had no obvious injury to cartilage cells, and the apoptosis rate was not significantly different from that of Control group. M1-SMG promoted apoptosis, with significantly higher apoptotic rate than that of Control and SMG groups. Comparison with Control, *P #P C) IF staining showed that there was no significant expression of Caspase-3 in Control or SMG group. The expression of Caspase-3 was up-regulated in M1-SMG, with significantly enhanced fluorescence intensity than that of SMG and Control. (D–E) Western-Blot (n = 3) Detection of protein expression showed that M1-SMG promoted the expression of apoptotic protein (Bax and Caspase-3) and inhibited the expression of Bcl-2. Comparison with Control, *P #P

Figure 4. M1-SMG induced cartilage cell injury. (AB) The results of flow cytometry showed that SMG had no obvious injury to cartilage cells, and the apoptosis rate was not significantly different from that of Control group. M1-SMG promoted apoptosis, with significantly higher apoptotic rate than that of Control and SMG groups. Comparison with Control, *P < 0.05; Comparison with SMG, #P < 0.05. (C) IF staining showed that there was no significant expression of Caspase-3 in Control or SMG group. The expression of Caspase-3 was up-regulated in M1-SMG, with significantly enhanced fluorescence intensity than that of SMG and Control. (DE) Western-Blot (n = 3) Detection of protein expression showed that M1-SMG promoted the expression of apoptotic protein (Bax and Caspase-3) and inhibited the expression of Bcl-2. Comparison with Control, *P < 0.05; Comparison with SMG, #P < 0.05.