Green tea polyphenol epigallocatechi3-gallate: Inflammation and arthritis

Abstract

A number of factors including inflammation and oxidative stress are believed to play a role in the development of chronic joint diseases. Green tea has become a popular drink and is consumed throughout the world. Extracts of green tea and polyphenols present therein have been shown to inhibit the inflammatory responses in vitro in different cell types and the development of arthritis in animal model studies. There is considerable evidence that (-)-epigallocatechin-3-gallate (EGCG), the predominant green tea polyphenol which mimic its effects, inhibits enzyme activities and signal transduction pathways that play important roles in inflammation and joint destruction in arthritis. After oral consumption EGCG become bioavailable and proteomic studies suggest that EGCG may directly interact with a large set of protein targets and alter the physiological response of the cells. Taken together these and other studies identify and support the use of EGCG as a possible chemopreventive agent with a potential to inhibit the development of arthritis. Here we review the biological effects of EGCG in an attempt to understand its pivotal molecular targets that directly affect the inflammation and joint destruction process for prevention and/or for the development of new therapeutics for arthritis in humans.

(−)-Epigallocatechin gallate but not chlorogenic acid upregulates osteoprotegerin synthesis through regulation of bone morphogenetic protein-4 in osteoblasts

“…CGA has been documented to increase mineralization in rat tibia and improve mechanical properties of the femoral diaphysis (11). In addition, CGA may suppress osteoclastic bone resorption by downregulating the effects of RANK ligand (12 osteoblastic bone formation (13,14), and green tea consumption may be associated with reduced age-related bone loss and fractures in the elderly (13). However, the underlying molecular mechanisms regarding the effects of CGA and EGCG on bone metabolism are currently unknown.…”

The Occurrence, Fate and Biological Activities ofC-glycosyl Flavonoids in the Human Diet

“…These backbones are the flavan-3-ols, flavonols, flavones, flavanones, isoflavones, anthocyanidins and chalcones (Scalbert and Williamson, 2000), which are subsequently differentiated by the presence of functional moieties such as hydroxyl groups at multiple positions about the carbon backbone, allowing for a diverse array of possible structures. Whilst additional substitution, including O-and C-methylation (Erlund, 2004), prenylation (Stevens and Page, 2004), gallation (Singh et al, 2011), glucuronidation (Hegnauer and Gpayer-Barkmeijer, 1993) and polymerisation (Manach et al, 2004) at various positions about the backbone structure all also further expand the diversity of the flavonoid family, glycosylation is arguably the most significant single native structural feature in determining the pharmacokinetics of any flavonoid in the human diet. The addition of a sugar moiety is capable of fundamentally altering parent compound bioavailability following oral consumption by modulating critical physicochemical parameters such as structural polarity (Day et al, 2000).…”

Green Tea epigallocatechin-3-gallate Protects Against Oxidative Stress-Induced Nuclear Translocation of p53 and Apoptosis in Retinal Pigment Epithelial Cells, ARPE-19

“…Epigallocatechin-3-gallate (EGCG), the most abundant (40-60%) component of polyphenolic flavonoids in green tea, has been shown to possess a strong and active antioxidant, according to its two triphenolic groups in its molecular structure (Singh, Akhtar, & Haqqi, 2010;Weinreb, Mandel, Amit, & Youdim, 2004). EGCG has been shown to protect H 2 O 2 -induced oxidative stress in various types of cell such as PC12 cells (Koh et al, 2003), G93A motorneuron cells (Koh et al, 2004), auditory neurons (Xie, Liu, Zhu, Wu, & Ge, 2004) and INS-1 insulinoma cells (Kim et al, 2010) through different anti-apoptotic mechanisms.…”