Apitherapy, the therapeutic use of honeybee products, has been studied in a number of conditions including rheumatoid arthritis (RA). How bee venom works in this disease has been a mystery… until now.
A recent study investigated the molecular mechanisms behind bee venom's impact on rheumatoid arthritis (RA), a chronic, autoimmune inflammatory disease. It appears that melittin, a major component of bee venom is a powerful anti-inflammatory agent.
To gain a better understanding of bee venom's potential benefits for RA patients, the researchers examined its action in a rat model of rheumatoid arthritis. For rats with advanced RA, treatment with bee venom at very low doses resulted in dramatic reductions of tissue swelling and bone spur formation on affected paws. The authors surmised that " the anti-arthritic effects of bee venom are related to the anti-inflammatory effects of bee venom."
Next, the researchers examined the anti-inflammatory effects of bee venom on synovial cells, the cells that line the joints, obtained from human RA patients. They found melittin was able to block the expression of inflammatory genes, similar to the way non-steroidal anti-inflammatory drugs (NSAIDS) used to treat RA, act. 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. As a result, melittin is able to effectively inactivate inflammation in a very specific fashion.
The authors concluded, "The potency of melittin in the inhibition of the inflammatory response may be of great benefit in degenerative and inflammatory diseases such as RA. 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."
Park HJ, Lee SH, Son DJ, Oh KW, Kim KH, Song HS, Kim GJ, Oh GT, Yoon DY, Hong JT. Antiarthritic Effect of Bee Venom: Inhibition of Inflammation Mediator Generation by Suppression of NF-êB Through Interaction With the p50 Subunit. Arthritis & Rheum. 2004; 50 (11): 3504-3515.
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