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Science Daily —
A new study from the University of Michigan Health
System suggests that a compound in green tea may provide therapeutic
benefits to people with rheumatoid arthritis.
The study, presented
April 29 at the Experimental Biology 2007 in Washington, D.C., looks at
a potent anti-inflammatory compound derived from green tea. Researchers
found that the compound – called epigallocatechin-3-gallate (EGCG) –
inhibited the production of several molecules in the immune system that
contribute to inflammation and joint damage in people with rheumatoid
arthritis.
The compound from green
tea also was found to suppress the inflammatory products in the
connective tissue of people with rheumatoid arthritis.
“Our research is a very
promising step in the search for therapies for the joint destruction
experienced by people who have rheumatoid arthritis,” says Salah-uddin
Ahmed, Ph.D., lead researcher on the study. Ahmed, a research
investigator with the Division of Rheumatology at the U-M Health System,
was selected to present the research at the Experimental Biology meeting
as the recipient of the Young Scientist Travel Award, given by the
American Society for Pharmacology and Experimental Therapeutics. This
study was also selected by the American Society for Nutrition to be
featured in a press release.
To conduct the research,
the scientists isolated cells called synovial fibroblasts from the
joints of patients with rheumatoid arthritis. These fibroblasts – cells
that form a lining of the tissue surrounding the capsule of the joints –
then were cultured in a growth medium and incubated with the green tea
compound.
The fibroblasts were then
stimulated with pro-inflammatory cytokine IL-1b, a protein of the immune
system known to play an important role in causing joint destruction in
people with rheumatoid arthritis. The researchers looked at whether the
green tea compound has the capability to block the activity of two
potent molecules, IL-6 and cyclooxygenase-2 (COX-2), which also are
actively involved in causing boneerosion in the joints of people with
rheumatoid arthritis.
When untreated cells were
stimulated with IL-1b, 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 inhibiting
the production of these molecules. EGCG also inhibited the production of
prostaglandin E2, a hormone-like substance that causes inflammation in
the joints.
The cell signaling
pathways that regulate levels of these immune system molecules under
both normal and rheumatoid arthritis situations are well studied, and
the researchers were able to trace the effects of the green tea compound
infusion to see that it worked by inhibiting these pathways.
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 by inhibiting the joint destruction in rheumatoid arthritis.
Previously, Ahmed and
other researchers made another promising finding when EGCG-pretreated
synovial fibroblasts were stimulated with the cytokine IL-1b to study
the protective effect of this green tea compound. Compared to untreated
synovial fibroblasts, the cells treated with EGCG markedly blocked the
ability of IL-1b to produce the proteins and enzymes that infiltrate the
joints of persons with rheumatoid arthritis and cause cartilage
degradation.
The laboratory now is
focused on the inhibitory role of EGCG in gene expression. The
scientists plan to test EGCG in animal models of rheumatoid arthritis to
see if it provides similar therapeutic or preventive effects. Ahmed
believes that the outcome of these studies will form a strong foundation
for future testing of green tea compound in humans with rheumatoid
arthritis.
In addition to Ahmed,
authors of the study are Angela Pakozdi, M.D., a former research fellow
in the Division of Rheumatology at the U-M Health System; and Alisa E.
Koch, M.D., the Frederick G.L. Huetwell and William D. Robinson, M.D.
Professor of Rheumatology at the U-M Health System and a researcher at
the Veterans Affairs Ann Arbor Healthcare System.
This research was
supported by National Institutes of Health grants and Veteran
Administration Medical Research Service funds to Koch.
Note: This story has
been adapted from a news release issued by University of Michigan Health
System. |
