• Journal of the Society of Cosmetic Scientists of Korea
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• v.34 no.2
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• pp.93-99
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• 2008

Until now, (-)-epigallocatechin-3-gallate(EGCG) is known as the most powerful antioxidant among green tea catechins having many beneficial effects on human skin. Considering that the content of catechins is variable according to many conditions such as solvent, temperature and pressure, we prepared the heat-epimerized-EGCG-mixture (HE-EGCG-mix) containing high content of gallocatechin-3-gallate(GCG) by epimerization during autoclaving process and found out its optimal condition for maximizing conversion from EGCG to GCG. To investigate the effects of EGCG and HE-EGCG-mix on skin barrier function, we performed in vivo experiments with hairless mice. We found that HE-EGCG-mix has more potent stimulating activity than EGCG for the production of involucrin 7(INV7) and for recovery of barrier function in SKH-1 mice. Also, we found that GCG stimulates $PPAR-{\alpha}$ transactivation more effectively than EGCG in vitro by transient transfection assay for $PPAR-{\alpha}$ activation activity. These imply that HE-EGCG-mix consisting of high content of GCG should stimulate more efficiently recovery of skin barrier through PPAR-mediated-kerationocyte differentiation than EGCG. In conclusion, our study may provide a possibility that GCG, the C-2 epimer of EGCG, could be a potentially effective agent for development of new cosmetics or health foods for recovery of skin barrier.

• Archives of Pharmacal Research
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• v.27 no.3
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• pp.334-339
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• 2004

In this study, the effects of (-)-epigallocatechin-3-gallate (EGCG) and/or hinokitiol (${\beta}-thujaplicin$) on melanogenesis were investigated. Our results showed that both EGCG and hinokitiol significantly inhibited melanin synthesis in a concentration-dependent manner, and that their hypopigmenting effects were stronger than that of kojic acid, which is known to inhibit melanin formation in melanocytes and melanoma cells. Interestingly, EGCG did not show any additive hypopigmenting effect in combination with kojic acid, though EGCG did show a synergistic effect in combination with hinokitiol. Several reports indicate that the activation of extracellular signal-regulated kinase (ERK) induces microphthalmia-associated transcription factor (MITF) degradation. Accordingly, the effects of EGCG and hinokitiol on the ERK signaling pathway were examined. EGCG and hinokitiol induced neither ERK activation nor MITF degradation. On the other hand, both EGCG and hinokitiol reduced the protein levels of MITF and of tyrosinase, the rate limiting melanogenic enzyme, whereas kojic acid had no effect. In addition, hinokitiol strongly downregulated the activity of tyrosinase, whereas EGCG or kojic acid had only a little effect. These results show that both EGCG and hinokitiol reduce MITF production, and suggest that reduced tyrosinase activity by hinokitiol explains their synergistic effect on melanogenesis.

• Natural Product Sciences
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• v.10 no.5
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• pp.228-236
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• 2004

The aim of the present study was to examine whether green tea extract (CUMC6335) affects the blood pressure and the isolated aortic contractility of the rabbit in comparison with one of the most powerful active catechins, epigallocatechin gallate (EGCG). The phenylephrine $(1-10\;{\mu}M)-induced$ contractile responses were greatly inhibited in the presence of CUMC6335 (0.3-1.2 mg/ml). Also, high potassium (56 mM)-induced contractile responses were depressed in high concentration (0.6-1.2 mg/ml), but not affected in low concentration CUMC6335 (0.3 mg/ml). However, epigallocatechin gallate $(EGCG,\;4-12\;{\mu}g/ml)$ did not affect the contractile responses evoked by phenylephrine and high $K^+$. The infusion of CUMC6335 with a rate of 20 mg/kg/30 min made a significant reduction in pressor responses induced by intravenous norepinephrine. However, EGCG (1 mg/kg/30 min) did not affect them. Collectively, these results obtained from the present study suggest that intravenous CUMC6335 causes depressor action in the anesthetized rat at least partly through the blockade of adrenergic ${\alpha}_1-receptors$. CUMC6335 also causes the relaxation in the isolated aortic strips of the rabbit partly via the blockade of adrenergic ${\alpha}_1-receptors$, in addition to the unknown direct mechanism. It seems that there is no species difference in the vascular effect between the rat and the rabbit.

• Journal of the Korean Society of Food Science and Nutrition
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• v.21 no.4
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• pp.386-389
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• 1992

The four main tea catechin components (-)-epicatechin (EC), (-)-epigallocatechin (EGC) , (-)-epicatechin gallate (ECg), and (-)-epigallocatechin gallate (EGCg) were analyzed quantitatively from commerical green teas by HPLC. CATechin of the most amounts in steamed and parched teas was EGcg (steamed 1st : 7.54% , parched 1st : 7.88%). Amounts of catechins decreased in the following order : EGCg > EGC>ECg>EC. Almost same tendency of catechin components change of 1st tea and 2nd tea differed to harvesting time being observed in steamed and parched teas. In 2nd tea, amounts of EGCg increased more than in 1st tea. It seems that this change effects on the quality of tea taste.

• The Journal of the Korean dental association
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• v.54 no.4
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• pp.284-295
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• 2016

The aim of this study was to evaluate the effect of Epigallocatechin-3-Gallate (EGCG) on the alveolar bone metabolism in a collagen-induced arthritis (CIA) model in mice to enhance the understanding of rheumatoid arthritis (RA)-associated alveolar bone loss. Following the induction of CIA in animals (mice, n=16), mandibles were retrieved for micro-computed tomography (micro-CT) and isolation of alveolar bone cells (ABCs). In vitro osteogenic potentials of ABCs were evaluated and the mRNA expression of downstream effector genes was assessed. CIA was successfully induced in all animals, and micro-CT data showed that alveolar bone loss was significantly increased in the CIA group while the treatment of EGCG prevented the alveolar bone resorption. Osteogenesis by ABCs was significantly increased in the CIA+EGCG group in vitro. The analysis of mRNA expressions showed that osteoclastogenesis-associated genes were increased in CIA group while bone protecting genes were upregulated in EGCG treated group. The results demonstrate that EGCG downregulated the alveolar bone resorption in a CIA model in mice, and upregulation of bone protecting genes appear to be involved. Further studies are warranted.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.41-51
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• 2016

Adult hippocampal dentate granule neurons are generated from neural stem cells (NSCs) in the mammalian brain, and the fate specification of adult NSCs is precisely controlled by the local niches and environment, such as the subventricular zone (SVZ), dentate gyrus (DG), and Toll-like receptors (TLRs). Epigallocatechin-3-gallate (EGCG) is the main polyphenolic flavonoid in green tea that has neuroprotective activities, but there is no clear understanding of the role of EGCG in adult neurogenesis in the DG after neuroinflammation. Here, we investigate the effect and the mechanism of EGCG on adult neurogenesis impaired by lipopolysaccharides (LPS). LPS-induced neuroinflammation inhibited adult neurogenesis by suppressing the proliferation and differentiation of neural stem cells in the DG, which was indicated by the decreased number of Bromodeoxyuridine (BrdU)-, Doublecortin (DCX)- and Neuronal Nuclei (NeuN)-positive cells. In addition, microglia were recruited with activating TLR4-NF-${\kappa}B$ signaling in the adult hippocampus by LPS injection. Treating LPS-injured mice with EGCG restored the proliferation and differentiation of NSCs in the DG, which were decreased by LPS, and EGCG treatment also ameliorated the apoptosis of NSCs. Moreover, pro-inflammatory cytokine production induced by LPS was attenuated by EGCG treatment through modulating the TLR4-NF-${\kappa}B$ pathway. These results illustrate that EGCG has a beneficial effect on impaired adult neurogenesis caused by LPS-induced neuroinflammation, and it may be applicable as a therapeutic agent against neurodegenerative disorders caused by inflammation.

• Journal of Nutrition and Health
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• v.44 no.3
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• pp.196-202
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• 2011

Epigallocatechin gallate (EGCG), or epigallocatechin 3-gallate, is the ester of epigallocatechin and gallic acid, and is a type of catechin. EGCG may be therapeutic for many disorders including diabetics and some types of cancer. However it is unknown whether EGCG can induce transdifferentiation of pancreatic cells in pancreatitis. The aim of this study was to investigate the effects of EGCG on the expression of pancreatic regenerating related markers in pancreatic AR42J cells, a model of pancreatic progenitor cells. AR42J cells, differentiated with betacellulin and activin A, were cultured with/without EGCG in a time-dependent manner. Cell growth rate, levels of mRNA, and protein expression were examined with the MTT assay, quantitative PCR, and Western blots, respectively. The results showed that AR42J cell growth rates were inhibited by EGCG in a dose-dependent manner. mRNA and protein expression of amylase, insulin and neurogenin 3 (ngn 3) increased in AR42J cells treated with EGCG. Additionally, we demonstrated that the signal transduction pathway of mitogen-activated protein (MAP) kinase is active in EGCG-treated AR42J cells. ERK and JNK phosphorylation decreased in cells treated with EGCG but not p38 phosphorylation. Activation of the p38 MAP kinase pathway was confirmed by specific MAP kinase pathways inhibitors: U0126 for ERK, SP600126 for JNK, and SB203580 for p38. Activated p38 phosphorylation was inhibited by the specific p38 inhibitor SB203580 but p38 phosphorylation was inhibited with increased EGCG treatment. The ERK and JNK MAP kinase pathways were not affected by EGCG treatment. Although further studies are needed, these results suggest that EGCG affects the induction of pancreatic cell regeneration by increasing the ngn 3 protein and mRNA expression and activating the p38 MAP kinase pathway.

• 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.

• Korean Journal of Head & Neck Oncology
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• v.27 no.1
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• pp.3-11
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• 2011

Hepatocyte growth factor(HGF) and c-Met play an important role in the control of tumor growth and invasion, and they are known to be good prognostic indicators of patient outcome. Epigallocatechin-3-gallate (EGCG) has been shown to have chemopreventive and therapeutic properties by modulating multiple signal pathways regarding the control of proliferation and invasion of cells. In this study, we evaluated the role of c-Met in EGCG-induced inhibition of invasion and apoptosis in an oral cancer cell line. In KB cells where c-Met was knocked down with siRNA, we performed invasion assay and FACS with Annexin V-FITC/PT staining. In addition, we checked the change of mitochondrial membrane potential(MMP) and the generation of reactive oxygen species(ROS). EGCG-induced inhibition of invasiveness was significantly decreased after the knock-down of c-Met. EGCG-induced apoptosis, MMP change and ROS generation was also reduced in c-Met knock-ed-down KB cells. These results suggest that c-Met is involved in EGCG-induced apoptosis and inhibition of invasiveness of oral cancer cell line.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.203-210
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• 2015

AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism. Previous studies have shown that activation of AMPK results in suppression of cardiac myocyte hypertrophy via inhibition of the p70S6 kinase (p70S6K) and eukaryotic elongation factor-2 (eEF2) signaling pathways. Epigallocatechin-3-gallate (EGCG), the major polyphenol found in green tea, possesses multiple protective effects on the cardiovascular system including cardiac hypertrophy. However, the molecular mechanisms has not been well investigated. In this study, we found that EGCG could significantly reduce natriuretic peptides type A (Nppa), brain natriuretic polypeptide (BNP) mRNA expression and decrease cell surface area in H9C2 cardiomyocytes stimulated with phenylephrine (PE). Moreover, we showed that AMPK is activated in H9C2 cardiomyocytes by EGCG, and AMPK-dependent pathway participates in the inhibitory effects of EGCG on cardiac hypertrophy. Taken together, our findings provide the first evidence that the effect of EGCG against cardiac hypertrophy may be attributed to its activation on AMPK-dependent signaling pathway, suggesting the therapeutic potential of EGCG on the prevention of cardiac remodeling in patients with pressure overload hypertrophy.