EGCG Molecule from Green Tea

Chemical structure Epigallocatechin gallate(EGCG), also known as epigallocatechin 3-gallate, is the ester of epigallocatechin and gallic acid, and is a type of catechin.

Molecular formula C22H18O11

Molar mass 458.37 g mol-1

Medicinal Properties

EGCG is the most abundant catechin in tea and is a potent antioxidant that may have therapeutic applications in the treatment of many disorders (e.g. cancer). It is found in green - but not black - tea, as EGCG is converted into thearubigins in black teas. In a high temperature environment, an epimerization change is more likely to occur; however as exposure to boiling water for 30 straight minutes only leads to a 12.4% reduction in the total amount of EGCG, the amount lost in a brief exposure is insignificant. In fact, even when special conditions were used to create temperatures well over that of boiling water, the amount lost scaled up only slightly.EGCG can be found in many supplements.

EGCG

A recent study using mouse models at the University of Southern California showed that, in contrast to the myriad benefits commonly associated with green tea and green tea extract (GTE), EGCG binds with the anti-cancer drug Velcade, significantly reducing its bioavailability and thereby rendering it therapeutically useless. Dr. Schönthal, who headed the study, suggests that consumption of green tea and GTE products be strongly contraindicated for patients undergoing treatment for multiple myeloma and mantle cell lymphoma. EGCG has a slight stimulatory effect due to it increasing adrenaline levels. Epigallocatechin-3-gallate, may reduce the bioavaialbilty of the drug sunitinib when they are taken together.

EGCG was, among other tea polyphenols, found to be a strong topoisomerase inhibitor, similar to some chemotherapeutic anticancer drugs, for example, etoposide and doxorubicin. This property may be responsible for anticarcinogenic however also a carcinogenic potential of the substance. High intake of polyphenolic compounds during pregnancy is suspected to increase risk of neonatal leukemia. Bioflavonoid supplements should not be used by pregnant women.A strong association between high intake of tea during pregnancy and elevated risk of childhood malignant central nervous system (CNS) tumours was found.

Bioavailability of EGCG

The bioavailability of the most abundant and most active green tea antioxidant, epigallocatechin gallate (EGCG) remains uncertain. see abstracts below....

Abstracts:

19 Nov 2018 -- Epigallocatechin gallate suppresses premature senescence of preadipocytes by inhibition of PI3K/Akt/mTOR pathway and induces senescent cell death by regulation of Bax/Bcl-2 pathway.

The phytochemical epigallocatechin gallate (EGCG) has been reported to alleviate age-associated immune disorders and organ dysfunction. However, information regarding the mechanistic role of EGCG in the suppression of cellular senescence is limited. The present study thus assessed the effects and underlying mechanisms of EGCG in the inhibition of senescence as well as its potential to selectively eliminate senescent cells (senolytics) using 3T3-L1 preadipocytes. Premature senescence was established in cells by repeated exposure of H2O2 at a sub-lethal concentration (150 μM). H2O2 treated cells showed characteristic senescence-associated features including increased cell size, senescence-associated β-galactosidase activity (SA-β-gal), development of senescence-associated secretory phenotype (SASP), activation of reactive oxygen species (ROS) and pathways, DNA damage as well as induction of cell cycle inhibitors (p53/p21WAF1/p16INK4a). In addition, a robust activation of PI3K/Akt/mTOR and AMPK pathways was also observed in H2O2 treated cells. Presence of EGCG (50 and 100 μM) showed significant downregulation of PI3K/Akt/mTOR and AMPK signaling along with the suppression of ROS, iNOS, Cox-2, NF-κB, SASP and p53 mediated cell cycle inhibition in preadipocytes. In addition, EGCG treatment also suppressed the accumulation of anti-apoptotic protein Bcl-2 in senescent cells thereby promoting apoptosis mediated cell death. Our results collectively show that EGCG acts as an mTOR inhibitor, SASP modulator as well as a potential senolytic agent thereby indicating its multi-faceted attributes that could be useful for developing anti-aging or age-delaying therapies. source

27 May 2015 Food Inhibits the Oral Bioavailability of the Major Green Tea Antioxidant Epigallocatechin Gallate in Humans

The bioavailability of the most abundant and most active green tea antioxidant, epigallocatechin gallate (EGCG) remains uncertain. Therefore, the systemic absorption of EGCG was tested in healthy fasted humans. It was administered as capsules with water or with a light breakfast, or when incorporated within a strawberry sorbet. The results for plasma EGCG clearly revealed that taking EGCG capsules without food was better; the AUC was 2.7 and 3.9 times higher than when EGCG capsules were taken with a light breakfast (p = 0.044) or with EGCG imbedded in the strawberry sorbet (p = 0.019), respectively. This pattern was also observed for Cmax and Cav. Therefore, ingesting food at the same time as EGCG, whether it was imbedded or not in food, substantially inhibited the absorption of the catechin. As with some types of medications that are affected by food, it appears that EGCG should be taken without food in order to maximise its systemic absorption. Therefore, based on these findings, ingesting EGCG with water on an empty stomach is the most appropriate method for the oral delivery of EGCG in clinical trials where EGCG is to be investigated as a potential bioactive nutraceutical in humans. see full publication

8 October 2012 -- Preventive Effects of Epigallocatechin-3-O-Gallate againstReplicative Senescence Associated with p53 Acetylation in HumanDermal Fibroblasts

Considering the various pharmacological activities of epigallocatechin-3-O-gallate (EGCG) including anticancer, and anti-inflammatory, antidiabetic, and so forth, relatively less attention has been paid to the antiaging effectofEGCGonprimarycells.In this study, the preventive effects of EGCG against serial passage-induced senescence were investigated in primary cells includingrat vascular smooth muscle cells (RVSMCs), human dermal fibroblasts (HDFs), and human articular chondrocytes (HACs). Theinvolvement of Sirt1 and acetylated p53 was examined as an underlying mechanism for the senescence preventive activity of EGCGin HDFs. All cells were employed with the initial passage number (PN) between 3 and 7. For inducing senescence, the cells wereserially passaged at the predetermined times and intervals in the absence or presence of EGCG (50 or 100μM). Serial passage-induced senescence in RVSMCs and HACs was able to be significantly prevented at 50μM EGCG, while in HDFs, 100μMEGCGcould significantly prevent senescence and recover their cell cycle progression close to the normal level. Furthermore, EGCG wasfound to prevent serial passage- and H2O2-induced senescence in HDFs by suppressing p53 acetylation, but the Sirt1 activity wasunaffected. In addition, proliferating HDFs showed similar cellular uptake of FITC-conjugated EGCG into the cytoplasm withtheir senescent counterparts but different nuclear translocation of it from them, which would partly account for the differentialresponses to EGCG in proliferating versus senescent cells. Taking these results into consideration, it is suggested that EGCG maybe exploited to craft strategies for the development of an antiaging or age-delaying agent.