Abstract
Rheumatoid arthritis (RA) is a refractory systemic autoimmune disease associated with synovial inflammation. Previous studies postulate that paeonol has good anti-arthritis effects on RA. However, its systematic description remains unknown. Herein, we used bioinformatics tools to evaluate the mechanism of paeonol in arthritis systematically. A macrophage model was employed to study the differentially expressed genes between the inflammation and normal group, revealing 169 inflammation-related genes. Another 275 key genes affected by paeonol were identified in the same model. Three key genes, FPR2, Cd83, and Cfb, were obtained after combining the two data sets. Paeonol inhibited the release of inflammatory factors and the proliferation of synovial. However, its inhibitory effect was blocked by Fpr2 blocker WRW4. In summary, paeonol can inhibit the development of arthritis through FPR2. This provides new scope for the design and development of FPR2 ligands.
Novel formyl peptide receptor (FPR) agonists with pyridinone and pyrimidindione scaffolds that are potentially useful for the treatment of rheumatoid arthritis
