Rheumatoid arthritis (RA) is an autoimmune disease in which cartilage in the joints is inflamed and leads to bone mass reduction. RA can also cause inflammation of organs. The reason RA exists is the body’s production of antibodies toward its own tissue, or attacking itself. White blood cells infiltrate the joints and organs causing inflammation, and bone loss. Chemokines are a group of proteins that among other actions, cause inflammation and can play a role in infectious diseases and cancer.
To control RA researchers have concentrated on stopping chemokine activity and the inflammation the protein is responsible for. The site of the protein activity is in cells called fibroblasts that make and distribute collagen in the body. When the body turns against itself and overproduces collagen in the fibroblasts causing inflammation, the result can be RA.
A catechin in green tea (from the Camellia sinensis plant), epigallocatechin-3-gallate (EGCG) has been studied as an anti-inflammatory agent because it can regulate proteins and enzymes responsible for various cell growth factors. Pakozdi and Koch reported that
EGCG reduced the activity of a specific protein labeled MCP-1.1 They also found another specific protein that EGCG blocked labeled MCP-2. Finally, EGCG inhibited activation and distribution of joint fibroblasts, leading to reduced production of collagen. These results indicate a possible use of EGCG for inhibiting the causes of joint inflammation and destruction in RA.
Scientists reported in 2010 that green tea extract (GTE) suppressed cartilage production and inhibited the production of proteins that activate white blood cells.2 Research in human models is needed to verify GTE as a viable anti-inflammatory therapy for RA.
Green Tea and Osteoarthritis
Osteoarthritis (OA) is an inflammatory disease that is primarily age-related. Cartilage cells are activated by certain metabolic products to produce cartilage. Under normal conditions, these cells are responsible for balancing growth and destruction of cartilage structure and tissue functioning. OA develops when abnormal cartilage production and degradation activities occur. It is not well-known what causes these conditions, but researchers are finding pieces of the OA puzzle regularly. A recent clue is that anti-aging therapy may play a supporting role in OA treatment. 3 Aigner and others concluded in 2007 targets for future study include therapies that regulate cartilage synthesis and destruction, give anti-inflammatory qualities to cells and regulate cell death.4
Epigallocatechin-3-gallate (EGCG), due to its previously reported anti-inflammatory qualities, has been tested for use in treating OA. A 2009 journal article reported success in using natural or synthetic EGCG to treat OA. The authors concluded that treatment with EGCG has potential to prevent cartilage destruction by repressing the production of proteins and metabolic products ultimately result in joint inflammation.3 Additional targets for future study include anti-aging strategies might complement existing therapies related to anabolism, catabolism, inflammation, and apoptosis-processes that are integral to the pathogenesis of osteoarthritis.
A study reported in early 2010 the potential anti-inflammatory benefits of a combination of avocado and soybean oils (known as ASU) with EGCG.5 The researchers used an equine model and found an enhanced anti-inflammatory effect on cartilage-producing cells when EGCG and ASU were given together. They concluded that the combination may be a useful therapy for OA.
1Regulation of interleukin-1beta-induced chemokine production and matrix metalloproteinase 2 activation by epigallocatechin-3-gallate in rheumatoid arthritis synovial fibroblasts. Ahmed S, Pakozdi A, Koch AE. Arthritis Rheum. 2006. 54(8):2393-2401.
2Green tea extract inhibits chemokine production, but up-regulates chemokine receptor expression, in rheumatoid arthritis synovial fibroblasts and rat adjuvant-induced arthritis
H. Marotte, J. H. Ruth, P. L. Campbell, A. E. Koch, S. Ahmed. Rheumatology. 2010. 49(3): 467-79.
3Green tea polyphenol epigallocatechin-3-gallate inhibits advanced glycation end product-induced expression of tumor necrosis factor-alpha and matrix metalloproteinase-13 in human chondrocytes. Rasheed, Z; Anbazhagan, AN; Akhtar, N; Ramamurthy, S; Voss, FR and Haqqi, TM. Arthritis Res Ther. 2009. 11(3):R71.
4Mechanisms of disease: role of chondrocytes in the pathogenesis of osteoarthritis–structure, chaos and senescence. Aigner, T; Söder, S; Gebhard, PM; McAlinden, A and Haag, J. Nat Clin Pract Rheumatol. 2007. 3(7):391-9.
5Inhibition of cyclooxygenase-2 expression and prostaglandin E2 production in chondrocytes by avocado soybean unsaponifiables and epigallocatechin gallate. Heinecke LF, Grzanna MW, Au AY, Mochal CA, Rashmir-Raven A, Frondoza CG. Osteoarthritis Cartilage. 2010. 18(2):220-7.
