Inhibitory effects of ginsenosides on S100 protein‐mediated rheumatic diseases

Rheumatoid arthritis(RA) is a chronic autoimmune disorder that primarily affects joints. It causes severe long‐term damage to various organ systems and results in progressive disability, systemic complications. The cause of rheumatoid arthritis is not well understood but involves a complex interplay of exogenous and endogenous inflammatory factors. Especially, numerous evidence show that S100 family also known as the pro‐inflammatory calcium‐binding protein, plays a pivotal role in the pathogenesis of rheumatic diseases. Some S100 proteins are released at the site of inflammation and participate in inflammatory signalling pathways via a variety of receptors. Therefore, these S100 proteins could be useful biomarkers for clinical joint damage in RA. Ginsenosides are a class of natural product steroid glycosides and triterpene saponins, which has a long history of use in traditional medicine. It has also been used in clinical practice for resolution of inflammation. In this study, we measured that RAW264.7 murine macrophage cell line and murine BMDMs are transfected or treated with S100 in presence of ginsenosides. The levels of cytokines were measured by ELISA. The results show that secretion of S100 proteins was inhibited by ginsenosides and pro‐inflammatory cytokines was decreased at the site of inflammation. Taken together, we suggested that pro‐inflammatory signaling of S100 proteins is inhibited by ginsenoside and this result indicated that effect of ginsenoside in S100‐mediated inflammation might be potential therapeutic target for resolving rheumatoid disease. Support or Funding Information This work was supported by the NRF grant funded by the Korea government (MSIP) 2019R1I1A2A01064237