Kim Mi-Sun, Yi Jin-Mu, Kim Sung Hoon, Hong Seung-Heon, Kim Hyung Min
Department of Pharmacology, College of Oriental Medicine, Kyung Hee University, 1 Hoegi-Dong, Dongdaemun-Gu, Seoul 130-701, South Korea.
Cytokine. 2004 Feb 21;25(4):179-86. doi: 10.1016/j.cyto.2003.11.016.
Madimadi, a Korean folk medicine, has been applied to treat rheumatoid arthritis (RA). However, its mechanisms of action have not been examined. The involvement of inflammatory cytokines, particularly TNF-alpha, IL-1beta, and IL-8, resulting in local inflammation in the pathogenesis of RA is now widely accepted. Madimadi dose-dependently inhibited TNF-alpha, IL-1beta, and IL-8 production from activated human mast cells (HMC-1). RT-PCR revealed inhibition of TNF-alpha and IL-1beta transcription in activated HMC-1. In addition, we confirmed potent inhibition of TNF-alpha and IL-1beta production by Madimadi using purified human blood PBMC from an active RA group, but not from healthy or disease control groups. These novel insights into the immunosuppressive action of Madimadi are likely to impact the clinical use of this agent.