• Journal of the Korean Society of Food Science and Nutrition
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• v.37 no.9
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• pp.1114-1119
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• 2008

Among the numerous polyphenols isolated from green tea, epigallocatechin gallate (EGCG) is a predominate and is considered to be a major therapeutic agent. To elucidate the mechanical insights of anti-tumor effect, EGCG was applied to human breast cancer MDA-MB-231 cells. We investigated the effect of EGCG on protein and mRNA expression of proteins related to cell apoptosis in MDA-MB-231 human breast cancer cell lines. We also identified caspase-3 activity. We cultured MDA-MB-231 cells in the presence of 0, 5, 10, and $20\;{\mu}M$ of EGCG. Protein and mRNA expression of bcl-2 were decreased dose-dependently in cells treated with EGCG. However, protein and mRNA expression of bax were increased (p<0.05). Caspase-3 activities were increased dose-dependently in cells treated with EGCG. These results suggest that EGCG induces cell apoptosis by increase of caspase activity through decreasing of protein and mRNA expression of bcl-2 and increasing of protein and mRNA expression of bax.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.8
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• pp.983-988
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• 2007

Epigallocatechin gallate (EGCG), a principal antioxidant derived from green tea, is one of the most extensively investigated chemopreventive phytochemicals. However, the effect of EGCG on proliferation in MDA-MB-231 breast cancer cell is not well known. We investigated the effect of EGCG on protein and mRNA expression related to cell proliferation in MDA-MB-231 human breast cancer cell lines. We cultured MDA-MB-231 cells in the presence of 0, 5, 10 and 20 ${\mu}m$ of EGCG. EGCG significantly inhibited the cancer cell proliferation (p<0.05). In MDA-MB-231 huamn breast cancer cell, EGCG lowered $ErbB_2$ and $ErbB_3$ protein as well as mRNA expression. In addition, protein and mRNA expression of phosphorylated Akt and total Akt were significantly decreased (p<0.05). We suggest that EGCG inhibits cell proliferation through $ErbB_2$, $ErbB_3$ and Akt cell signaling.

• Microbiology and Biotechnology Letters
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• v.44 no.1
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• pp.62-67
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• 2016

Hydrolytic enzyme activities, including those of ${\beta}$-glucosidase, ${\beta}$-glucuronidase, ${\beta}$-xylosidase, ${\beta}$-galactosidase, ${\beta}$-arabinofuranosidase, ${\beta}$-arabinosidase, and ${\beta}$-arabinopyranosidase, which are useful for bioconversion, were explored in lactic acid bacteria isolated from Korean traditional fermented foods. Nine bacterial strains were selected for the fermentation of green tea extract prepared by supercritical fluid extraction. Changes in the concentrations of catechin, epicatechin, epicatechin gallate, epigallocatechin, and epigallocatechin-3-gallate in green tea extract were investigated after fermentation by the selected lactic acid bacteria strains. The strain Leuconostoc mesenteroides MBE1424, which showed the highest ${\beta}$-glucuronidase enzyme activity among the tested bacterial strains, increased the epigallocatechin content of the green tea extract by 60%. In addition, L. mesenteroides MBE1424 was more resistant than the control strain at high temperature and showed a maximum specific growth rate at $40^{\circ}C$. L. mesenteroides MBE1424 was presumed to have an enzyme system containing ${\beta}$-glucuronidase with utility in the bioconversion of green tea extract.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.5
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• pp.259-266
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• 2011

The aim of this study was to evaluate the preventive role of epigallocatechin-3 gallate (EGCG, a derivative of green tea) in ischemia/reperfusion (I/R) injury of isolated rat hearts. It has been suggested that EGCG has beneficial health effects, including prevention of cancer and heart disease, and it is also a potent antioxidant. Rat hearts were subjected to 20 min of normoxia, 20 min of zero-flow ischemia and then 50 min of reperfusion. EGCG was perfused 10 min before ischemia and during the whole reperfusion period. EGCG significantly increased left ventricular developed pressure (LVDP) and increased maximum positive and negative dP/dt (+/-dP/dtmax). EGCG also significantly increased the coronary flow (CF) at baseline before ischemia and at the onset of the reperfusion period. Moreover, EGCG decreased left ventricular end diastolic pressure (LVEDP). This study showed that lipid peroxydation was inhibited and Mn-SOD and catalase expressions were increased in the presence of EGCG. In addition, EGCG increased levels of Bcl-2, Mn-superoxide dismutase (SOD), and catalase expression and decreased levels of Bax and increased the ratio of Bcl-2/Bax in isolated rat hearts. Cleaved caspase-3 was decreased after EGCG treatment. EGCG markedly decreased the infarct size while attenuating the increase in lactate dehydrogenase (LDH) levels in the effluent. In summary, we suggest that EGCG has a protective effect on I/R-associated hemodynamic alteration and injury by acting as an antioxidant and anti-apoptotic agent in one.

• Journal of Food Hygiene and Safety
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• v.22 no.3
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• pp.223-230
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• 2007

We have previously reported that green tea catechins(GTC) displayed potent antithrombotic effect, which was due to the antiplatelet activity. In the present study, the antiplatelet activity of each green tea catechin components was compared in vitro. Galloylated catechins including (-)-epigallocatechin gallate (EGCG), (-)-gallocatechin gallate (GCG), (-)-epicatechin gallate (ECG) and (-)-catechin gallate (CG), significantly inhibited collagen $(5{\mu}g/mL)-induced$ rabbit platelet aggregation with $IC_{50}$ values of 79.8, 63.0, 168.2 and $67.3{\mu}M$, respectively. EGCC GCG and CG also significantly inhibited arachidonic acid (AA, $100{\mu}M$)-induced rabbit platelet aggregation with $IC_{50}$ values of 98.9, 200.0 and $174.3{\mu}M$, respectively. However catechins without gallate moiety showed little inhibitory effects against rabbit platelet aggregation induced by collagen or AA compared with galloylated catechins. These observations suggest that the presence of gallate moiety at C-3 position may be essential to the antiplatelet activity of catechins and the presence of B ring galloyl structure may also contribute to the antiplatelet activity of GTC. In line with the inhibition of collagen-induced platelet aggregation, EGCG caused concentration-dependent decreases of cytosolic calcium mobilization, AA liberation and serotonin secretion. In contrast, epigallocatechin (EGC), a structural analogue of EGCG lacking a galloyl group in the 3' position, although slightly inhibited collagen-stimulated cytosolic calcium mobilization, failed to affect other signal transductions as EGCG in activated platelets. Taken together, these observations suggest that the antiplatelet activity of EGCG may be due to inhibition of arachidonic acid liberation and inhibition of $Ca^{2+}$ mobilization and that the antiplatelet of EGCG is enhanced by the presence of a gallate moiety esterified at carbon 3 on the C ring.

• Applied Biological Chemistry
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• v.35 no.4
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• pp.276-280
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• 1992

Quantutative analysis of catechins by HPLC was studied. When the mobile phase was switched from the conventional(AOAC) Methanol, Acetonitril and Acetic acid solution in $H_2O$ to 0.06% Phosphate solution with Acetonitrile, N,N-Dimethyl formamide, and Ethyl acetate, retention time could be reduced from 45 min to 28 min, especially, we obtained sharper chromatogram of the compounds, either (-)EGCG or (-)ECG, which resulted in minimization of analytical erros. CVs of retention time $(0.32{\sim}3.97%)$ and peak area $(1.61{\sim}7.01%)$ indicated that the data were more reliable. Content of catechins in commerical teas analyzed by the method was $120.3{\sim}153.7\;mg/g$ in green teas which was about 4 times that in black tea.

• Journal of Life Science
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• v.13 no.6
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• pp.924-932
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• 2003

Epigallocatechin-3 Gallate (EGCG), a major constituent of green tea, has attracted increasing interest because of its many reported health benefits. Here we demonstrate for the first time that EGCG stimulates phospholipase D (PLD) activity in U87 human astroglioma cells. EGCG-induced PLD activation was abolished by the phospholipase C (PLC) inhibitor and a lipase inactive PLC-\gama1$ mutant, and was dependent on intracellular $Ca^{ 2+}$, and possibly involved $Ca^{ 2+}$ calmodulin-dependent protein kinase II (CaM kinase II). Interestingly, EGCG induced translocation of PLC-\gama1$ from the cytosol to the membrane and PLC-\gama1$interaction with PLD1. Taken together, these results demonstrate for the first time that in human astroglioma cells, EGCG regulates PLD activity via a signaling pathway involving a PLC-\gama1$ (inositol 1,4,5-trisphosphate-$Ca^{ 2+}$)-CaM kinase II-PLD pathway.

• Korean Journal of Food Science and Technology
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• v.31 no.4
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• pp.1024-1028
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• 1999

Green tea infusions were prepared by extracting them with aqueous solution of different pHs and their physicochemical properties were analyzed. Yellowness, chroma and total color difference values were increased as pH increased. The content of total amino acids in the green tea infusion was not influenced by pH values. Total catechin contents of the green tea infusion extracted at pH 4.0, 5.0, 6.0 and 7.0 were 32.28, 31.84, 31.14 and 14.70 mg/g, respectively. Among the four catechins investigated, epigallocatechingallate and epigallocatechin are more unstable as the pH was changed from 6.0 to 7.0. As pH increased, the extraction of caffeine was also increased. In conclusion, extraction at low pH is preferred for the preparation of green tea infusion.

• Journal of Pharmaceutical Investigation
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• v.37 no.2
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• pp.107-111
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• 2007

Epigallocatechin gallate (EGCC), a flavonoid, is the main component of green tea extracts. EGCG has been reported to be an inhibitor of P-glycoprotein (P-gp) and cytochrom P450 3A(CYP3A4). This study investigated the effect of long-term administration of EGCG on the pharmacokinetics of verapamil in rats. Pharmacokinetic parameters of verapamil were determined after oral administration of verapamil (9 mg/kg) in rats pretreated with EGCG (7.5 mg/hg) for 3 and 9 days. Compared to oral control group, the presence of EGCG significantly (p<0.01) increased the area under the plasma concentration-time curve (AUC) of verapamil by 102% (coad), 83.2% (3 days) and 52.3% (9 days), and the peak concentration $(C_{max})$ by 134% (coad), 120% (3 days) and 66.1% (9 days). The absolute bioavailability (A.B.%) of verapamil was significantly (p<0.01) higher by 8.4% (coad), 7.7% (3 days), 6.4% (9 days) compared to control (4.2%), and presence of EGCG was no significant change in the terminal half-life $(t_{1/2})$ and the time to reach the peak concentration $(T_{max})$ of verapamil. Our results indicate that EGCG significantly enhanced oral bioavailability of verapamil in rats, implying that presence of EGCG could be effective to inhibit the CYP3A4-mediated metabolism and P-gp efflux of verapamil in the intestine. Drug interactions should be considered in the clinical setting when verapamil is coadministrated with EGCG or EGCG-containing dietary.

• Proceedings of the Korean Society of Plant Biotechnology Conference
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• 2004.10a
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• pp.74-79
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• 2004

Little is known about the effect of epigallocatechin-3 gallate (ESCG), a major constituent of green tea, on the expression of cyclooxygenase (COX)-2. Here, we studied the role of phospholipase D (PLD) isozymes in EGCG-induced COX-2 expression. Stimulation of human astrocytoma cells (U87) with EGCG induced formation of phosphatidylbutanol, a specific product of PLD activity, and synthesis of COX-2protein and its product, prostaglandin $E_2$ ($PGE_2$). Pretreatment of cells with 1-butanol, but not 3-butanol, suppressed EGCG-induced COX-2 expression and $PGE_2$ synthesis. Furthermore, evidence that PLD was involved in EGCG-induced COX-2 expression w3s provided by the observations that COX-2 expression was stimulated by over-expression of PLD1 or PLD2 isozymes and treatment with phosphatidic acid(PA), and that prevention of PA dephosphorylation by 1-propranolol significantly potentiated COX-2expression Induced by EGCG. EGCG induced activation of p38 mitogen-activated protein kinase (p38MAPK), and specific Inhibition of p38 MAPK dramatically abolished EGCG-Induced PLD activation, COX-2 expression, and $PGE_2$ formation. Moreover, protein kinase C (PKC) inhibition suppressed EGCG-induced p38 MAPK activation, COX-2 expression, and $PGE_2$ accumulation. The same pathways as those obtained in the astrocytoma cells were active in primary rat astrocytes, suggesting the relevance of the findings. Collectively, our results demonstrate for the first time that PLD isozymes mediate EGCG-induced COX-2 expression through PKC and p38 in immortalized astroglial line and normal astrocyte cells.