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Green tea compound suppresses factors causing cartilage, bone destruction in arthritis

filtrate the joints of persons with rheumatoid arthritis causing cartilage degradation.

The scientists decided to extend their study to see if the green tea compound also has the capability to block the activity of two other potent molecules, IL-6 and cyclooxygenase-2 (COX-2), actively involved in causing bone erosion in the RA joint. In the new study presented at Experimental Biology, the scientists once again isolated synovial fibroblasts taken from the joints of patients suffering from rheumatoid arthritis and incubated these cells with the green tea compound. When untreated cells were stimulated with IL-1, a sequence of molecular events occurred that resulted in production of the bone-destructive molecules. But the scientists found that pre-incubation with EGCG was capable of blocking the production of these molecules in a dose-dependent manner. Furthermore, EGCG also inhibited the production of prostaglandin E2, which causes inflammation in the joints.

The cell signaling pathways that regulate levels of these immune system molecules under both normal and rheumatoid arthritis situations is well established, and the researchers were able to trace the effects of the green tea compound infusion to see that it worked by inhibiting these pathways.

Dr. Ahmed says that these studies suggest that EGCG or molecules that could be derived synthetically from the EGCG found in green tea may be of therapeutic value in inhibiting the joint destruction in this challenging disease. The laboratory now is focused on the inhibitory role of EGCG in gene expression. The scientists plan to give EGCG orally to mice genetically bred to be animal models of rheumatoid arthritis to see if it provides similar therapeutic or preventive effects. Dr. Ahmed believes these studies will form a strong foundation for future testing of green tea compounds in humans with rheumatoid arthritis.


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Contact: Sylvia Wrobel
ebpress@bellsouth.net
770-270-0989
Federation of American Societies for Experimental Biology
29-Apr-2007


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