• YAKHAK HOEJI
• /
• v.45 no.1
• /
• pp.101-107
• /
• 2001

Green tea catechins (GTC) and its major component, (-)-epigallocatechin gallate (EGCG) were studied for their protective effects against reactive oxygen species (ROS)-induced oxidative stress. GTC and EGCG skewed the strong antioxidative effects on the lipid peroxidation of ethyl linolate with Fenton's reagent and free radical scavenging effect to DPPH radical generation. They also protected $H_2O$$_2$- or KO$_2$-induced cytotoxicity in CHL cells or mouse splenocytes. These results indicate that GTC and EGCG are capable of protecting the lipid peroxidation, flee radical generation and cytotoxicity induced by ROS. The mechanism of inhibition in ROS-induced cytotoxicity may be due to their antiofidative and free radical scavenging properties. Therefore, GTC and EGCG may be useful chemopreventive agents by protecting the free radical generation which are involved in cancer and aging.

• Korean Journal of Food Science and Technology
• /
• v.43 no.4
• /
• pp.483-489
• /
• 2011

Epigallocatechin-3-gallate (EGCG) is a polyphenolic compound frequently found in green tea, and its physiological actions have been extensively investigated. In the present study, changes in chemical stability and cytotoxic properties of EGCG in the presence of different types of antioxidants were investigated. The antioxidants used modulated the chemical stability of EGCG. Superoxide dismutase (SOD) significantly increased EGCG stability; EGCG was less stable in the presence of catalase. Ascorbic acid, N-acetylcysteine (NAC), and glutathione (GSH) stabilized EGCG concentration dependently. The $H_2O_2$ level generated from EGCG was decreased by catalase, SOD, and NAC but not by GSH. The cytotoxic effects of EGCG also decreased in the presence of NAC, catalase, and SOD. GSH, however, showed a complicated modulatory pattern according to the EGCG and GSH concentrations, and ascorbic acid rather enhanced EGCG toxicity. The results suggest that certain antioxidants could modulate the cytotoxic properties of EGCG in a cell culture system not only by removing reactive oxygen species but by modulating chemical stability and other factors, which should be considered carefully when studying reactive oxygen species-dependent mechanisms of EGCG.

• Natural Product Sciences
• /
• v.22 no.2
• /
• pp.87-92
• /
• 2016

Endothelial dysfunction in atherosclerosis is associated with increasing oxidative stress that could be reversed by antioxidant. Therefore epigallocatechin gallate (EGCG), epicatechin gallate (ECG), epigallocatechin (EGC) and catechin (C) of tea flavonoids were investigated for their roles in regenerating endothelial cell. Peripheral blood mononuclear cells (PB-MNCs) were isolated, plated and cultured in medium with/without treatment of EGCG, ECG, EGC and C. Results showed that among all EGCG, ECG, EGC and C concentrations tested, $12.5{\mu}mol/L$ was not cytotoxic for peripheral blood-derived endothelial progenitor cells (PB-EPCs). Treatment of EGCG, ECG, EGC or C increased the percentages of CD34, CD133, VEGFR-2 expressions and suppressed hydrogen peroxide-induced percentages of reactive oxygen species (ROS) level in PB-EPCs. Taken together, our current results showed that EGCG, ECG, EGC or C of tea flavonoids could induce differentiation of PB-MNCs into PB-EPCs as well as protect PB-EPCs from oxidative damage by suppresing the intracellular ROS levels.

• Journal of Veterinary Science
• /
• v.23 no.5
• /
• pp.74.1-74.16
• /
• 2022

Background: Previous studies have presented evidence to support the significant association between red meat intake and colon cancer, suggesting that heme iron plays a key role in colon carcinogenesis. Epigallocatechin-3-gallate (EGCG), the major constituent of green tea, exhibits anti-oxidative and anti-cancer effects. However, the effect of EGCG on red meat-associated colon carcinogenesis is not well understood. Objectives: We aimed to investigate the regulatory effects of hemin and EGCG on colon carcinogenesis and the underlying mechanism of action. Methods: Hemin and EGCG were treated in Caco2 cells to perform the water-soluble tetrazolium salt-1 assay, lactate dehydrogenase release assay, reactive oxygen species (ROS) detection assay, real-time quantitative polymerase chain reaction and western blot. We investigated the regulatory effects of hemin and EGCG on an azoxymethane (AOM) and dextran sodium sulfate (DSS)-induced colon carcinogenesis mouse model. Results: In Caco2 cells, hemin increased cell proliferation and the expression of cell cycle regulatory proteins, and ROS levels. EGCG suppressed hemin-induced cell proliferation and cell cycle regulatory protein expression as well as mitochondrial ROS accumulation. Hemin increased nuclear factor erythroid-2-related factor 2 (Nrf2) expression, but decreased Keap1 expression. EGCG enhanced hemin-induced Nrf2 and antioxidant gene expression. Nrf2 inhibitor reversed EGCG reduced cell proliferation and cell cycle regulatory protein expression. In AOM/DSS mice, hemin treatment induced hyperplastic changes in colon tissues, inhibited by EGCG supplementation. EGCG reduced the hemin-induced numbers of total aberrant crypts and malondialdehyde concentration in the AOM/DSS model. Conclusions: We demonstrated that EGCG reduced hemin-induced proliferation and colon carcinogenesis through Nrf2-inhibited mitochondrial ROS accumulation.

• International Journal of Oral Biology
• /
• v.30 no.3
• /
• pp.77-84
• /
• 2005

EGCG[(-)-epigallocatechin gallate], is a major component of green tea has been considered as a major antioxidant constituent. It has been considered as potential chemopreventive and chemotherapeutic agents. However, very little is known about the cellular actions by which EGCG mediates its therapeutic effects. Various aspects of antioxidant activity of EGCG were evaluated in this study. EGCG itself did not show significant cytotoxicity. Significant 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity was observed in all ranges of concentration ($0.8-100{\mu}g/ml$) used in this study. Protective effect of EGCG against hydrogen peroxide induced cell death was observed. Relatively high lipid peroxidation inhibitory activity were detected ($IC_{50}$ was about $20{\mu}g/ml$). EGCG also dose-dependently enhanced the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in V79-4 cells. In concentrations of $100{\mu}g/ml$ of EGCG, activities of SOD, CAT and GPX were measured as 36.9 U/mg of protein, 22.9 U/mg of protein and 17.8 U/mg of protein, respectively. When these values were compared with those of the control groups (24.9 U/mg of protein, 14.9 U/mg of protein and 11.7 U/mg of protein), the relative increases were calculated as 48, 54 and 52%, respectively. Taken together, our findings suggest that EGCG can act as an antioxidant by scavenging radicals and enhancing antioxidant enzyme activities.

• The Korean Journal of Food And Nutrition
• /
• v.30 no.5
• /
• pp.1035-1041
• /
• 2017

(-)-Epigallocatechin-3-gallate (EGCG) is a major catechin found in green tea. It is reported that EGCG possesses various health benefits including anti-cancer, antioxidant, anti-diabetes, and anti-obesity. The objective of this study was to investigate the effects of EGCG on adipogenesis via activation of AMP-activated protein kinase (AMPK) pathway in 3T3-L1 preadipocytes. In order to determine the effects of EGCG on adipogenesis, preadipocyte differentiation was induced in the presence or absence of EGCG ($0{\sim}100{\mu}M$) for a period of 6 days. EGCG significantly inhibited fat accumulation and suppressed the expression of adipogenic specific proteins including peroxisome proliferator-activated receptor (PPAR)-${\gamma}$. Also, EGCG markedly increased the activation of AMPK and acetyl-CoA carboxylase (ACC) and the production of intracellular reactive oxygen species (ROS). However, any pretreatment with a specific AMPK inhibitor, compound C, abolished the inhibitory effects of the EGCG on $PPAR{\gamma}$ expression. This study suggests that EGCG has anti-adipogenic effects through modulation of the AMPK signaling pathway and therefore, may be a promising antiobesity agent.

• Asian-Australasian Journal of Animal Sciences
• /
• v.31 no.9
• /
• pp.1420-1430
• /
• 2018

Objective: Epigallocatechin-3-gallate (EGCG) is a major ingredient of catechin polyphenols and is considered one of the most promising bioactive compounds in green tea because of its strong antioxidant properties. However, the protective role of EGCG in bovine oocyte in vitro maturation (IVM) has not been investigated. Therefore, we aimed to study the effects of EGCG on IVM of bovine oocytes. Methods: Bovine oocytes were treated with different concentrations of EGCG (0, 25, 50, 100, and $200{\mu}M$), and the nuclear and cytoplasmic maturation, cumulus cell expansion, intracellular reactive oxygen species (ROS) levels, total antioxidant capacity, the early apoptosis and the developmental competence of in vitro fertilized embryos were measured. The mRNA abundances of antioxidant genes (nuclear factor erythriod-2 related factor 2 [NRF2], superoxide dismutase 1 [SOD1], catalase [CAT], and glutathione peroxidase 4 [GPX4]) in matured bovine oocytes were also quantified. Results: Nuclear maturation which is characterized by first polar body extrusion, and cytoplasmic maturation characterized by peripheral and cortical distribution of cortical granules and homogeneous mitochondrial distribution were significantly improved in the $50{\mu}M$ EGCG-treated group compared with the control group. Adding $50{\mu}M$ EGCG to the maturation medium significantly increased the cumulus cell expansion index and upregulated the mRNA levels of cumulus cell expansion-related genes (hyaluronan synthase 2, tumor necrosis factor alpha induced protein 6, pentraxin 3, and prostaglandin 2). Both the intracellular ROS level and the early apoptotic rate of matured oocytes were significantly decreased in the $50{\mu}M$ EGCG group, and the total antioxidant ability was markedly enhanced. Additionally, both the cleavage and blastocyst rates were significantly higher in the $50{\mu}M$ EGCG-treated oocytes after in vitro fertilization than in the control oocytes. The mRNA abundance of NRF2, SOD1, CAT, and GPX4 were significantly increased in the $50{\mu}M$ EGCG-treated oocytes. Conclusion: In conclusion, $50{\mu}M$ EGCG can improve the bovine oocyte maturation, and the protective role of EGCG may be correlated with its antioxidative property.

• The Korean Journal of Physiology and Pharmacology
• /
• v.14 no.5
• /
• pp.325-329
• /
• 2010

Vascular NADPH oxidase plays a pivotal role in producing superoxide in endothelial cells and thus acts in the initiation and development of inflammatory cardiovascular diseases such as atherosclerosis. Epigallocatechin-3-gallate (EGCG), the major catechin derived from green tea, has multiple beneficial effects for treating cardiovascular disease but the effect of EGCG on the expression of vascular NADPH oxidase remains unknown. In this study, we investigated the mechanism(s) by which EGCG might inhibit the expression of subunits of NADPH oxidase, namely $p47^{phox}$, $p67^{phox}$ and $p22^{phox}$, induced by angiotensin II (Ang II) in human umbilical vein endothelial cells. Ang II increased the expression levels of $p47^{phox}$, $p67^{phox}$, and $p22^{phox}$, but EGCG counteracted this effect on $p47^{phox}$. Moreover, EGCG did not affect the production of reactive oxygen species induced by Ang II. These data suggest a novel mechanism whereby EGCG might provide direct vascular benefits for treating inflammatory cardiovascular diseases.

• Food Science and Biotechnology
• /
• v.18 no.4
• /
• pp.971-977
• /
• 2009

The most abundant tea catechin, epigallocatechin-3-gallate (EGCG), has been reported to inhibit cell proliferation and induce apoptosis in many types of cancer cells. In the present study, effects of EGCG on the growth of oral epithelial cells including CAL-27 oral squamous carcinoma cells and dysplastic oral keratinocytes (DOK) were investigated. EGCG inhibited growth of CAL-27 cells and DOK with $IC_{50}$ of 14.4-21.0 and 5.8-14.2 ${\mu}M$ after 24 and 48 hr incubation, respectively. EGCG was significantly less effective in inhibiting DOK growth. The effects of EGCG, however, were dramatically less pronounced in the presence of superoxide dismutase (SOD) and catalase. Inhibitory effects of EGCG on CAL-27 cell growth were also much less pronounced in the presence of fetal bovine serum (FBS). EGCG induced caspase-3 activation in both CAL-27 and DOK cells in a serum free condition without SOD/catalase; in the presence of 10% FBS and SOD/catalase, EGCG, even at 100 ${\mu}M$, did not affect cell growth. The present results indicate that EGCG inhibited oral cell growth with higher potency to more malignant CAL-27 cells than DOK, and the effects were markedly altered by SOD/catalase and serum content in media.

• International Journal of Oral Biology
• /
• v.45 no.4
• /
• pp.179-189
• /
• 2020

Green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) is a potent antioxidant with protective effects against neurotoxicity. However, it is currently unclear whether EGCG protects neuronal cells against radiation-induced damage. Therefore, the objective of this study was to investigate the effects of EGCG on ultraviolet (UV)-induced oxidative stress and apoptosis in PC12 cells. The effects of UV irradiation included apoptotic cell death, which was associated with DNA fragmentation, reactive oxygen species (ROS) production, enhanced caspase-3 and caspase-9 activity, and poly (ADP-ribose) polymerase cleavage. UV irradiation also increased the Bax/Bcl-2 ratio and mitochondrial pathway-associated cytochrome c expression. However, pretreatment with EGCG before UV exposure markedly decreased UV-induced DNA fragmentation and ROS production. Furthermore, the UV irradiation-induced increase in Bax/Bcl-2 ratio, cytochrome c upregulation, and caspase-3 and caspase-9 activation were each ameliorated by EGCG pretreatment. Additionally, EGCG suppressed UV-induced phosphorylation of p38 and rescued UV-downregulated phosphorylation of ERK. Taken together, these results suggest that EGCG prevents UV irradiation-induced apoptosis in PC12 cells by scavenging ROS and inhibiting the mitochondrial pathways known to play a crucial role in apoptosis. In addition, EGCG inhibits UV-induced apoptosis via JNK inactivation and ERK activation in PC12 cells. Thus, EGCG represents a potential neuroprotective agent that could be applied to prevent neuronal cell death induced by UV irradiation.