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Nutrition, Vitamins & Supplements for Seniors
Green Tea May be a Therapy for People with
Rheumatoid Arthritis
Anti-inflammatory compound inhibits destruction of
cartilage, bone
 April 30, 2007 - 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. 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.
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.
"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-1ƒÒ, 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 bone erosion in the joints of people with rheumatoid
arthritis.
When untreated cells were stimulated with IL-1ƒÒ, 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-1ƒÒ 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-1ƒÒ 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.
Editor's Notes:
Original report written by: Katie Gazella
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.
Dr. Ahmed's Experimental Biology presentation was
part of the scientific program of the American Society for Nutrition.
This research was supported by National Institutes
of Health grants and Veteran Administration Medical Research Service
funds to Koch.
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