A team of researchers in South Korea recently conducted an investigation into the molecular mechanisms behind bee venom's therapeutic impact on RA, a chronic, destructive inflammatory disease. The November 2004 issue of Arthritis & Rheumatism (http://www.
To gain a better understanding of bee venom's potential benefits for RA patients, the researchers examined its action in rat treated to induce inflammatory arthritis. For rats with advanced RA, treatment with bee venom at very low doses resulted in dramatic reductions of tissue swelling and osteophyte formation on affected paws. "Although the issue for determination of an effective dose is needed for further study," observes one of the authors, Jin Tae Hong, M.D., Ph.D. "Our data show that the anti-arthritic effects of bee venom are related to the anti-inflammatory effects of bee venom."
In the next phase of their study, researchers examined the anti-inflammatory effects of bee venom on synovial cells - cells lining the joints- obtained from human RA patients. Their experiments focused on melittin, bee venom's principal peptide. They observed melittin's power to block the expression of inflammatory genes, much like COX-2 inhibitor drugs used to treat RA. Melittin effectively reduces inflammation by inhibiting the critical DNA binding activity of NF-kB (Nuclear Factor kappa B), which directly controls a number of genes involved in immune reactions. Thus, Melittin's targeted inactivation of inflammation may hold the key to the anti-arthritic effects of bee venom.
"The potency of melittin in the inhibition of the inflammatory response may be of great benefit in degenerative and inflammatory diseases such as RA," concludes Dr. Hong. "The extent of inhibitory effects of melittin in most parameters determined in the present study is similar to or greater than bee venom itself, suggesting that melittin may be a major causative component in the pharmacologic effects of bee venom."
Article: "Antiarthritic Effect of Bee Venom: Inhibition of Inflammation Mediator Generation by Suppression of NF-êB Through Interaction With the p50 Subunit," Hye Ji Park, Seong Ho Lee, Dong Ju Son, Ki Wan Oh, Ki Hyun Kim, Ho Seub Song, Goon Joung Kim, Goo Taeg Oh, Do Young Yoon, and Jin Tae Hong, Arthritis & Rheumatism, November 2004; 50:11; pp. 3504-3515 (DOI: 10.1002/art.20626).