Study Elucidates Mechanisms and Effects of Green Tea Antioxidant on Arthritis
September 18, 2015
Elena Watts
Chandra Mohan

The Journal of Inflammation recently published a paper co-authored by Chandra Mohan, professor of biomedical engineering at UH Cullen College, about the effects of green tea on chronic autoimmune arthritis in mice.

Rheumatoid arthritis, RA, is the most common form of autoimmune arthritis, and women account for about 75 percent of the more than 1.3 million Americans affected, according to the American College of Rheumatology website.

The chronic disease that causes pain, stiffness, swelling and limited motion in joints has no known cure, but conventional drug therapies and experimental treatments can slow its progression. Unfortunately, these treatments have limited efficacy and serious side effects, so researchers are exploring herbal products such as green tea that have shown promise for treating the inflammatory autoimmune disease.

Past studies have suggested that an antioxidant, EGCG, found in green tea modulates arms of the immune system, so the purpose of this study was to examine EGCG mechanisms of action and the effects of those actions on collagen-induced arthritis in mice. Mohan and his collaborators at the University of Texas Southwestern Medical Center in Dallas and the Rheumatism Center at Inha University School of Medicine in South Korea conducted their study in two groups of arthritic mice. They administered the green tea antioxidant to the experimental group, and they gave phosphate buffered saline to the control group.

The researchers observed that EGCG treatment improved clinical symptoms, reduced indicators of disease activity and decreased antibody levels associated with progression of the disease in the experimental group, unlike overall outcomes in the control group. Their study revealed that EGCG treatment suppressed expansion of B and T immune cell populations, which contribute to the development of autoimmune arthritis, by slowing frequency and reducing absolute numbers of cells. They also found that the antioxidant treatment significantly decreased inflammation-related cytokine production and increased production of anti-inflammatory cytokine.

While prior studies have reported correlations between reduction of EGCG activity and escalation of the autoimmune disease, theirs was the first to report a relationship between EGCG treatment and induced expression of a target enzyme, an activity previously shown to increase antioxidant activity that protects against joint destruction in mice with arthritis.

Antioxidant activity that results in increased levels of the target enzyme was a significant discovery because researchers have shown that pharmacological upregulation of the target enzyme causes robust anti-inflammatory response in non-autoimmune arthritis animal models. Their findings provide new insights about EGCG mechanisms and perhaps a novel target for therapeutic treatment of chronic inflammatory diseases for future models.

“Further studies are required to determine the clinical relevance of these findings and to conduct systematic testing of potential therapeutic targets in this regulatory cascade,” the authors wrote in their paper. “It remains to be established whether EGCG is useful for the prevention and treatment of rheumatoid arthritis and other inflammatory disorders.”

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