Disease relevance of Epicatechin

• Microarray-assisted pathway analysis identifies mitogen-activated protein kinase signaling as a mediator of resistance to the green tea polyphenol epigallocatechin 3-gallate in her-2/neu-overexpressing breast cancer cells [1].
• CLINICAL IMPLICATIONS: Epigallocatechin gallate has potential use as adjunctive therapy in HIV-1 infection [2].
• Rats were administered 100 mg/kg body weight/d epicatechin orally for 1, 5, and 10 d [3].
• Inhibition of penicillinase by epigallocatechin gallate resulting in restoration of antibacterial activity of penicillin against penicillinase-producing Staphylococcus aureus [4].
• No association between urinary levels of epicatechin or its metabolite and colon cancer risk was observed [5].

Psychiatry related information on Epicatechin

• After exclusion of cases diagnosed under 4 years follow-up, urinary EGC positivity showed a statistically significant inverse association with gastric cancer (OR = 0.52, 95% CI = 0.28-0.97) after adjustment for Helicobactor pylori seropositivity, smoking, alcohol drinking, and level of serum carotenes [6].

High impact information on Epicatechin

• Inhibition of skin tumor promoter-caused induction of epidermal ornithine decarboxylase in SENCAR mice by polyphenolic fraction isolated from green tea and its individual epicatechin derivatives [7].
• Constitutive Overexpression of Nrf2-dependent Heme Oxygenase-1 in A549 Cells Contributes to Resistance to Apoptosis Induced by Epigallocatechin 3-Gallate [8].
• The intermediate filament protein vimentin is a new target for epigallocatechin gallate [9].
• Phospholipase D isozymes mediate epigallocatechin gallate-induced cyclooxygenase-2 expression in astrocyte cells [10].
• Administration of dexamethasone, epigallocatechin gallate, alpha-phenyl-N-tert-butyl nitrone, and ebselen significantly suppressed iNOS transgene induction by IFN-gamma and LPS [11].

Chemical compound and disease context of Epicatechin

• BACKGROUND: The green tea flavonoid, epigallocatechin gallate (EGCG), has been proposed to have an anti-HIV-1 effect by preventing the binding of HIV-1 glycoprotein (gp) 120 to the CD4 molecule on T cells [2].
• The catechin epigallocatechin gallate, one of the main constituents of green tea, showed strong antibiotic activity against 18 isolates of Stenotrophomonas maltophilia (MIC range, 4 to 256 microg/ml) [12].
• We investigated the proteolytic mechanisms for apoptosis in human malignant (N-type) neuroblastoma SH-SY5Y cells following exposure to flavonoids such as apigenin (APG), (-)-epigallocatechin (EGC), (-)-epigallocatechin-3-gallate (EGCG) and genistein (GST) [13].
• From these preliminary cytotoxicity assays (MTT) we found that C8-propyl-catechin gallate was more active (IC50 = 31 microM) than catechin gallate (CG, IC50 = 53 microM) or epicatechin gallate (ECG, IC50 = 76 microM) against the colorectal adenocarcinoma cell line HCT116 [14].
• Activity of the tea component epicatechin gallate and analogues against methicillin-resistant Staphylococcus aureus [15].

Biological context of Epicatechin

• Contrasting influences of glucuronidation and O-methylation of epicatechin on hydrogen peroxide-induced cell death in neurons and fibroblasts [16].
• We consider the cytotoxicity and the protection against oxidative stress for members of the naphthalenediol family and the known antioxidant epigallocatechin gallate (EGCG) [17].
• There is considerable interest in the bioavailability of epicatechin after oral ingestion [3].
• We conclude that under these experimental conditions, quercetin, catechin, and epicatechin do not suppress lipid peroxidation in vivo [18].
• Pharmacokinetics and safety of green tea polyphenols after multiple-dose administration of epigallocatechin gallate and polyphenon E in healthy individuals [19].

Anatomical context of Epicatechin

• Effects of epicatechin on rat islets of Langerhans [20].
• Epicatechin and its methylated metabolite attenuate UVA-induced oxidative damage to human skin fibroblasts [21].
• Although, epicatechin was transferred across the jejunum of the small intestine yielding metabolites, its nitroso form was not absorbed [22].
• Epigallocatechin gallate, the main polyphenol in green tea, binds to the T-cell receptor, CD4: Potential for HIV-1 therapy [2].
• Dimer B2 but not epicatechin monomer inhibited the proliferation of, and triggered apoptosis in, Caco-2 cells [22].

Associations of Epicatechin with other chemical compounds

• Analysis of Arabidopsis PA and its precursors indicates that Arabidopsis, unlike many other plants, exclusively uses the epicatechin and not the catechin pathway to PA [23].
• Experimental Designs: Thirty healthy volunteers were randomly assigned to one of the following doses of Polyphenon E (a decaffeinated and defined green tea catechin mixture): 400, 800, or 1,200 mg, based on the epigallocatechin gallate content (10 subjects per dose group) [24].
• In contrast, endothelial function at baseline correlated with dietary flavonoid intake (beta = 0.32, P = 0.02) and with baseline plasma EC concentration after adjusting for confounding variables (beta = 0.39, P = 0.03) [25].
• CONCLUSIONS: Cocoa flavanol and procyanidin supplementation for 28 d significantly increased plasma epicatechin and catechin concentrations and significantly decreased platelet function [26].
• The pharmacokinetics of the conjugated metabolites of epigallocatechin and epicatechin were not affected by repeated green tea polyphenol treatment [19].

Gene context of Epicatechin

• We found that epigallocatechin (EGCG) decreases VEGF receptor phosphorylation and induces apoptosis in CLL B cells [27].
• OxLDL stimulated a Ca(2+)-dependent activation of both ERK1/2 and JNK that was strongly inhibited by pre-treatment with low micromolar concentrations of epicatechin [28].
• Epigallocatechin suppression of proliferation of vascular smooth muscle cells: correlation with c-jun and JNK [29].
• When H4IIE cells were treated with epigallocatechin gallate, a green tea constituent, an increase in SHARP-2 mRNA levels and a decrease in PEPCK mRNA levels were observed [30].
• We also present new data on the inhibition of SULT1A enzymes by dietary chemicals, showing that compounds to which we are exposed regularly, such as epigallocatechin gallate and epicatechin gallate are extremely potent inhibitors of phenol sulfotransferases (K(i) in the nanomolar range for SULT1A1) [31].

Analytical, diagnostic and therapeutic context of Epicatechin

• Intraperitoneal injection of 30 mg/kg body wt of epicatechin twice daily for 4 days increased the islet insulin content by 30% [20].
• Employing HPLC followed by comparison with authentic standards for retention times in HPLC profiles, physiochemical properties and spectral analysis, nine individual polyphenols were identified as catechin, epicatechin, procyanidins B1-B5 and C1 and procyanidin B5-3'-gallate [32].
• Unexpectedly, epicatechin gallate (ECG), which has Fe(III)-reducing potency comparable with EGCG, failed to decrease the viability of Jurkat cells, while epigallocatechin (EGC), which has low capacity to reduce Fe(III), showed cytotoxic effects similar to EGCG [33].
• Black tea extracts (hot aqueous, polyphenols and theaflavins) and green tea extracts (hot aqueous, polyphenols, epicatechin, epicatechin gallate, epigallocatechin and epigallocatechin gallate) were tested in nine standardized cell culture assays for comparative cancer chemopreventive properties [34].
• The resulting biosensors were finally applied to the determination of epicatechin and ferulic acid as flavonol and polyphenol model, respectively [35].

References