| Uses |
(-)-Epigallocatechin Gallate is a tumor-inhibiting constituent of green tea. (-)-Epigallocatechin Gallate alters the cleavage of amyloid precursor protein, decreasing production of amaloid-ß and amaloid plaques in mice. This compound has neuroprotective properties. |
| Chemical Properties |
solid |
| Uses |
telomerase inhibitor |
| Uses |
An inhibitor of Bcl-2 and NOS2 |
| Uses |
A tumor-inhibiting constituent of green tea. Alters the cleavage of amyloid precursor protein, decreasing production of amaloid- and amaloid plaques in mice |
| Hazard |
Moderately toxic by ingestion. |
| Anticancer Research |
EGCG and EGC are the active polyphenol compounds found in green tea, found toinhibit p-glycoprotein transport activities in Chinese hamster ovary (p-gp+) cells.EGCG facilitates the retraction of MDR phenotype by reducing cellular drug effluxwhen given in combination with vinblastine or doxorubicin. Hesperetin, quercetin,daidzein, silymarin, naringenin, and resveratrol also inhibit the MRP1, MRP4, andMRP5 (Kawasaki et al. 2008). Curcumin increases the cellular accumulation ofanticancer agents like cisplatin, tamoxifen, daunorubicin, vincristine, anddoxorubicin and thereby effectively sensitizes the drug-resistant cancer cells. Areduction in MDR1B expression in L1210/Adr cells (mouse leukemic MDR cells)by curcumin is mediated by PI3K, Akt, and NF-κB pathways. It also inhibits theABCG2 transporter activity. In addition curcumin facilitates the accumulation ofmitoxantrone and doxorubicin in ABCG2-expressing HEK cells and hence reversesMDR (Kawasaki et al. 2008; Dandawate et al. 2013). |
| Anticancer Research |
EGCG is an ester of gallic acid and epigallocatechin and is a catechin compound(Murakami et al. 1996). It is found most abundantly in green tea. It can be used to treat brain, prostate, cervical, and bladder cancers (Wang et al. 2012). It suppressesthe ornithine decarboxylase action, an enzyme that leads to rapid proliferation andfurthermore circumvents apoptosis (Singh et al. 2016a). It suppresses nuclear factor(NF-κB) activation and expression of Bcl-2 (B-cell lymphoma 2) as well as COX-2(cyclooxygenase-2) in prostate cancer cells and causes induction of apoptosis. Ithamper the matrix metallopeptidase-9 (MMP-9) activation in bladder and lungcancer cells and suppresses the synthesis of VGEF (vascular endothelial growthfactor) in head and neck cancers. It prevents ERK (extracellular signal-regulatedkinase) phosphorylation and MMP-2 and MMP-9 activation and suppresses ERK,c-Jun N-terminal kinase (JNK), and MMP-9 expressions in gastric carcinoma cells(Singh et al. 2016a). It is binding and inhibits the antiapoptotic protein Bcl-xL,interferes with EGFR (epidermal growth factor receptor) signaling, and inhibitshepatocyte growth factor-induced cell proliferation and MAPK (mitogen-activatedprotein kinase), CDK (cyclin-dependent kinase), and cell signaling linked to growthfactors (Wang et al. 2012; Du et al. 2012).
Green tea constitutes the rich amount of EGCG which aids in cancer chemoprevention(Fujiki et al. 1998). EGCG improved the impacts of ginseng compoundin the restraint of colon tumor cell development, showing that green tea could bea successful synergist with an anticancer agent for malignancy chemoprevention.It obstructs the PDGF-initiated proliferation and migration of rodent pancreaticstellate cells (Masamune et al. 2005). The soluble and plasma membrane-integratedEGCG straightforwardly communicates with PDGF-BB and in this wayputs off precise receptor binding promoting the inhibitory impacts of EGCG onplatelet-derivedgrowth factor-incited cell signaling and mitogens (Weber et al.2004). |
