Abstract
Green tea has been shown to have beneficial effects on many diseases such as cancer, obesity, inflammatory diseases, and neurodegenerative disorders. The major green tea component, epigallocatechin-3-O-gallate (EGCG), has been demonstrated to contribute to these effects through its anti-oxidative and pro-oxidative properties. Furthermore, several lines of evidence have indicated that the binding affinity of EGCG to specific proteins may explain its mechanism of action. This review article aims to reveal how EGCG-protein interactions can explain the mechanism by which green tea/EGCG can exhibit health beneficial effects. We conducted a literature search, using mainly the PubMed database. The results showed that several methods such as dot assays, affinity gel chromatography, surface plasmon resonance, computational docking analyses, and X-ray crystallography have been used for this purpose. These studies have provided evidence to show how EGCG can fit or occupy the position in or near functional sites and induce a conformational change, including a quaternary conformational change in some cases. Active site blocking, steric hindrance by binding of EGCG near an active site or induced conformational change appeared to cause inhibition of enzymatic activity and other biological activities of proteins, which are related to EGCG’s biological oligomer and formation of their toxic aggregates, leading to the prevention of neurodegenerative diseases and amyloidosis. In conclusion, these studies have provided useful information on the action of green tea/catechins and would lead to future studies that will provide further evidence for rational EGCG therapy and use EGCG as a lead compound for drug design.
Highlights
Green tea has been shown to have beneficial effects on many diseases such as cancer, metabolic syndrome (MetS), inflammatory diseases, and neurodegenerative disorders [1,2,3,4,5,6,7]
These findings suggest that EGCG’s direct binding of pro-inflammatory chemokines and resultant inhibition of recruit of inflammatory cells is involved in its anti-inflammatory mechanism and warranted further development of EGCG as a potent therapeutic for inflammatory diseases [51]
EGCG inhibited P38 and NFκB expression, whereas EC and EGC were not effective inhibitors. These findings suggest that EGCG is the most effective catechin in inhibiting downstream inflammatory signaling, but its effectiveness could be hindered by the presence of EC
Summary
Green tea has been shown to have beneficial effects on many diseases such as cancer, metabolic syndrome (MetS), inflammatory diseases, and neurodegenerative disorders [1,2,3,4,5,6,7]. Scholey et al found that EGCG administration induced a significant overall increase in α, β and θ activity, and increased self-rated calmness and reduced self-rated stress [11] These findings encourage further studies on green tea/catechins; clarification of the action mechanisms including those associated with catechins–protein interactions will provide useful information which contributes to public health and the development of new drugs. EGCG can exert an anti-obesity effect through the activation of AMPK, leading to the down-regulation of sterol-response element binding proteins (SREBPs) which are the transcriptional factors to up-regulate the gene expression of two lipogenic enzymes: fatty acid synthase (FASN) and 3-hydroxy-3-methyglutaryl-CoA reductase (HMGR) These proteins are known as targets for cancer therapy [16,17]. The present review aims to update information from such studies on EGCG-protein interaction and discuss the molecular mechanism by which green tea may exert its health-promoting actions
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