In LPS-stimulated synoviocytes (obtained from patients with RA) under hypoxia, emodin significantly inhibited IL-1β and LPS-stimulated proliferation of RA synoviocytes, as well as the production of pro-inflammatory cytokines (TNFα, IL-6 and IL-8), mediators (PGE2), matrix metalloproteinase, which were related with the reduced histone deacetylase (HDAC) activity [111]. This evidence concerns the gene CXCL8 and rheumatoid arthritis.