Figure 6.

Enzyme-linked immunosorbent assay (ELISA) analysis of selected rheumatoid arthritis (RA)-related chondrocyte protein secretions in response to antirheumatic treatment. ELISA analysis confirmed the expression profiles of interleukin-6 (IL-6), interleukin-8 (CXCL-8/IL-8), and macrophage inflammatory protein-3α (CCL-20/MIP-3α) following treatment with azathioprine, gold sodium thiomalate, chloroquine phosphate, methotrexate, piroxicam, diclofenac, methylprednisolone, and prednisolone on the protein level. The secretion of the cytokines IL-6, CXCL-8/IL-8, and CCL-20/MIP-3α was induced in RASFsn-stimulated chondrocytes. All examined antirheumatic drugs significantly repressed the synthesis of IL-6 and CXCL-8/IL-8 (except for chloroquine phosphate) and repressed the synthesis of CCL-20/MIP-3α (except for chloroquine phosphate and diclofenac) in human chondrocytes, as already determined by microarray analysis. The mean of each triplicate well is plotted, and the error bars represent the standard deviation. Statistical analysis was performed for chondrocytes stimulated with supernatant of antirheumatically treated rheumatoid arthritis synovial fibroblasts (RASFs) compared the untreated condition (*P < 0.05). DMARD, disease-modifying antirheumatic drug; NSAID, nonsteroidal anti-inflammatory drug; RASFsn, supernatant of untreated rheumatoid arthritis synovial fibroblast; SAID, steroidal anti-inflammatory drug.