• 제목/요약/키워드: epigallocatechin-3-gallate (EGCG)

검색결과 149건 처리시간 0.022초

Comparison of Antiplatelet Activities of Green Tea Catechins

  • Cho, Mi-Ra;Jin, Yong-Ri;Lee, Jung-Jin;Lim, Yong;Kim, Tack-Joong;Oh, Ki-Wan;Yoo, Hwan-Soo;Yun, Yeo-Pyo
    • 한국식품위생안전성학회지
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    • 제22권3호
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    • pp.223-230
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    • 2007
  • 저자들은 녹차 카테킨(GTC)이 강한 항 혈전 작용을 나타내며, 이는 항 혈소판 활성에 의한 것임을 보고한 바 있다. 본 연구에서는, 8가지 녹차 카테킨 성분들의 항 혈소판 활성을 비교하였다. 실험결과, 갈레이트(gallate) 구조를 갖는 카테킨들(EGCG, GCG, ECG, CG)은 콜라겐$(5{\mu}g/ml)$으로 유도한 토끼 혈소판 응집능을 강하게 억제하였으며, 50% 억제농도$(IC_{50})$는 각각 79.8, 63.0, 168.2, $67.3{\mu}M$이었다. 또한 EGCG, GCG, CG는 아라키돈산(AA, $100{\mu}M$)으로 유도한 토끼 혈소판 응집능을 억제하였고, 50% 억제농도$(IC_{50})$는 각각 98.9, 200.0, $174.3{\mu}M$이었다. 반면에, 갈레이트 구조를 가지지 않는 카테킨들은 혈소판 응집능 억제 효과가 매우 약했다. 이 결과는 항 혈소판 활성에서 카테킨들의 C-3 위치의 갈레이트 구조의 존재가 매우 중요하다는 것과 카테킨들과 B-ring 갈레이트 구조의 존재 또한 녹차카테킨의 항 혈소판 활성에 중요한 작용한다는 것을 의미한다. 그리고, EGCG는 농도 의존적으로 세포내 칼슘 생성과 아리키돈산의 생성을 억제시켰는데, 이는 혈소판 응집능의 억제와 일치하였다. 반면에, EGC는 세포 내 칼슘 및 다른 혈소판 활성 기전에 아무런 영향이 없었다. 이들 결과는 EGCG의 항 혈소판 활성은 C-ring에서 carbon 3 자리의 에스테르화 된 갈레이트 구조의 존재에 의해서 강화된 항 혈소판 작용으로, 아라키돈산 생성과 세포 내 칼슘 생성을 억제하는 효과에 기인한 것이라 사료된다.

Effects of epigallocatechin-3-gallate on bovine oocytes matured in vitro

  • Huang, Ziqiang;Pang, Yunwei;Hao, Haisheng;Du, Weihua;Zhao, Xueming;Zhu, Huabin
    • Asian-Australasian Journal of Animal Sciences
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    • 제31권9호
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    • pp.1420-1430
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    • 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.

3T3-L1 Adipocyte에 인삼 사포닌과 EGCG (Epigallocatechin Gallate)처리가 Leptin, Hormone Sensitive Lipase, Resistin mRNA- 발현에 미치는 영향 (The Effects of Ginseng Saponin-Re, Re and Green Tea Catechine; ECGC (Epigallocatechin Gallate) on Leptin, Hormone Sensitive Lipase and Resistin mRNA Expressions in 3T3-L1 Adipocytes)

  • 김성옥;황은주;최원경
    • Journal of Nutrition and Health
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    • 제39권8호
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    • pp.748-755
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    • 2006
  • The purpose of this study was to find out effects of treatment of ginsenoside Re, Rc and EGCG on mRNA expressions of leptin, hormone sensitive lipase (HSL) and resistin in 3T3-L1 adipocytes. The concentrations of EGCG were treated with $0.01{\times}10^{-7},\;0.1{\times}10^{-7},\;1{\times}10^{-7}\;and\;1{\times}10^{-6}\;or\;100{\mu}g/ml$ ginsenoside Re, Rc in culture cell for 13 days. mRNA expression of leptin wasn't expressed in preadipocyte but according to differentiation of adipocyte, the that of mRNA expression was decreased at gensenosids or EGCG treated cells compared with non treated adipocyte. Expression of HSL mRNA was increased in G-Re, G-Rc and EGCG treated cells compared with non treated cells. The resistin level was significantly decreased in adipocytes treated with G-Re, G-Rc and EGCG. These pattern was similar to leptin expression. These results support that treatment of gensenosides or EGCG in 3T3-L1 adipocyte resulted to affect of leptin and resistin as well as HSL mRNA levels, accordingly, levels of leptin and HSL will be acted by signalling body fat stores to the hypothalamus which in turn regulates food intake andenergy expenditure to maintain body weight homeostasis. And also regulation of resistin mRNA will prevent to diabetics attacked with obesity. In conclusion, we suggest that consumption of ginseng saponine or EGCG might prevent human diabetics or/and obesity.

Effect of Purified Green Tea Catechins on Cytosolic Phospholipase $A_2$ and Arachidonic Acid Release in Human Gastrointestinal Cancer Cell Lines

  • Hong, Jung-Il;Yang, Chung-S.
    • Food Science and Biotechnology
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    • 제15권5호
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    • pp.799-804
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    • 2006
  • Ingestion of green tea has been shown to decrease prostaglandin $E_2$ levels in human colorectum, suggesting that tea constituents modulate arachidonic acid metabolism. In the present study, we investigated the effects of four purified green tea catechins, (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epigallocatechin-3-gallate (EGCG), and (-)-epicatechin-3-gallate (ECG), on the catalytic activity of cytosolic phospholipase $A_2$ ($cPLA_2$) and release of arachidonic acid and its metabolites from intact cells. At $50\;{\mu}M$, EGCG and ECG inhibited $cPLA_2$ activity by 19 and 37%, respectively, whereas EC and EGC were less effective. The inhibitory effects of these catechins on arachidonic acid metabolism in intact cells were much more pronounced. At $10\;{\mu}M$, EGCG and ECG inhibited the release of arachidonic acid and its metabolites by 50-70% in human colon adenocarcinoma cells (HT-29) and human esophageal squamous carcinoma cells (KYSE-190 and 450). EGCG and ECG also inhibited arachidonic acid release induced by A23187, a calcium ionophore, in both HT-29 and KYSE-450 cell lines by 30-50%. The inhibitory effects of green tea catechins on $cPLA_2$ and arachidonic acid release may provide a possible mechanism for the prevention of human gastrointestinal inflammation and cancers.

Epigallocatechin-3-gallate suppresses hemin-aggravated colon carcinogenesis through Nrf2-inhibited mitochondrial reactive oxygen species accumulation

  • Seok, Ju Hyung;Kim, Dae Hyun;Kim, Hye Jih;Jo, Hang Hyo;Kim, Eun Young;Jeong, Jae-Hwang;Park, Young Seok;Lee, Sang Hun;Kim, Dae Joong;Nam, Sang Yoon;Lee, Beom Jun;Lee, Hyun Jik
    • Journal of Veterinary Science
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    • 제23권5호
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    • pp.74.1-74.16
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    • 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.

Phospholipase D isozymes mediate epigallocatechin gallate-induced cyclooxygenase-2 expression in astrocyte cells

  • Kim, Shi-Yeon;Min, Kyoung-Jin;Joe, Eun-Hye;Min, Do-Sik
    • 한국식물생명공학회:학술대회논문집
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    • 한국식물생명공학회 2004년도 생명공학 실용화를 위한 비젼
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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.

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Protective Effect of Green Tea Extract and EGCG on Ethanol-induced Cytotoxicity and DNA Damage in NIH/3T3 and HepG2 Cells

  • Kim, Nam Yee;Kim, Hyun Pyo;Heo, Moon Young
    • 한국식품위생안전성학회지
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    • 제31권1호
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    • pp.1-7
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    • 2016
  • 본 연구의 목적은 NIH3T3와 HepG2 세포에서 에탄올 유도 세포독성 및 유전독성에 대하여 녹차엑기스(GTE)와 epigallocatechin-3-gallate (EGCG)의 보호작용을 평가하는데 있다. 세포생존율은 MTT assay를 실시하였으며 DNA 손상도는 Comet assay로 실시한 결과 에탄올은 농도의존적인 세포독성과 유전독성을 나타내었다. 한편 GTE와 EGCG는 에탄올 유도 세포독성 및 DNA 손상에 대하여 유의성 있는 억제효과를 나타내었으며 DPPH시험과 LDL oxidation 및 8OH-2'dG 생성시험에서 항산화효과를 나타내었다. 한편 녹차성분 함유 시판 리큐르주도 순수 에탄올에 비하여 세포독성억제 및 DNA 손상억제효과를 나타내었다. 이상의 시험결과 GTE와 함유 EGCG는 항산화성 유전독성억제기전을 통한 에탄올독성저감 물질로 판단된다.

Green tea polyphenol (-)-epigallocatechin-3-gallate prevents ultraviolet-induced apoptosis in PC12 cells

  • Woo, Su-Mi;Kim, Yoon-Jung;Cai, Bangrong;Park, Sam-Young;Kim, Young;Kim, Ok Joon;Kang, In-Chol;Kim, Won-Jae;Jung, Ji-Yeon
    • International Journal of Oral Biology
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    • 제45권4호
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    • pp.179-189
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    • 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.

Reversal of Cisplatin Resistance by Epigallocatechin Gallate Is Mediated by Downregulation of Axl and Tyro 3 Expression in Human Lung Cancer Cells

  • Kim, Kyung-Chan;Lee, ChuHee
    • The Korean Journal of Physiology and Pharmacology
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    • 제18권1호
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    • pp.61-66
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    • 2014
  • Lung cancer is still the number one cause of death from cancer worldwide. The clinical effect of platinum-based chemotherapy for non-small cell lung cancer is constrained by the resistance to drug. To overcome chemo-resistance, various modified treatment including combination therapy has been used, but overall survival has not been improved yet. In this study, chemo-resistant lung cancer cells, A549/Cis and H460/Cis, were developed by long-term exposure of cells to cisplatin and the proliferative capability of these resistant cells was verified to be reduced. We found cytotoxic effect of epigallocatechin gallate (EGCG), a major catechin derived from green tea, on both the parental lung cancer cells, A549 and H460, and their cisplatin resistant cells, A549/Cis and H460/Cis. ELISA and Western blot analysis revealed that EGCG was able to increase interlukine-6 (IL-6) production per cell, whereas its downstream effector Signal transducers and activators of transcription 3 (STAT3) phosphorylation was not changed by EGCG, indicating that IL-6/STAT3 axis is not the critical signaling to be inhibited by EGCG. We next found that EGCG suppresses the expression of both Axl and Tyro 3 receptor tyrosine kinases at mRNA and protein level, explaining the cytotoxic effect of EGCG on lung cancer cells, especially, regardless of cisplatin resistance. Taken together, these data suggest that EGCG impedes proliferation of lung cancer cells including their chemo-resistant variants through downregulation of Axl and Tyro 3 expression.

TREK-1 채널에 대한 플라보노이드의 효과 (The effect of flavonoids on the TREK-1 channel)

  • 김양미;김경아
    • 한국산학기술학회논문지
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    • 제12권6호
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    • pp.2660-2667
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    • 2011
  • TREK-1 채널은 two-pore 도메인 포타슘 (K2P) 채널로서 세포내 pH, 세포막의 신전, 불 포화 지방산, 온도, 휘발성 마취제, 신경세포방어물질에 의해 잘 조절된다. TREK-1 채널은 포타슘 이동에 의해 신경세포의 흥분성과 안정막전압을 조절한다. 최근 TREK-1은 전립선 암세포에서도 과발현됨이 확인되었다. 이러한 중요성에도 불구하고, TREK-1 채널에 대한 플라보노이드 효과는 거의 알려지지 않았다. 본 연구의 목적은 전기생리학적 방법 중의 하나인 excised inside-out patch기법을 이용하여 TREK-1 채널을 조절하는 플라보노이드를 탐색하는 것이다. TREK-1 채널이 발현된 CHO 세포에서 단일채널 팻취고정 방법을 이용하여 커큐민 (curcumin), EGCG (epigallocatechin-3-gallate), 퀘르세틴 (quercetin)에 의한 TREK-1 채널의 차단효과를 증명하였다. 퀘르세틴과 커큐민의 차단효과는 가역적으로 회복되었으나 EGCG는 거의 회복되지 않았다. 퀘르세틴, EGCG, 커큐민의 상대적 채널 활성도 (relative channel activity)는 $73{\pm}2.3%$ (n=5), $91{\pm}3.2%$ (n=7), $94{\pm}5.6%$ (n=4)까지 감소하였다. CHO 세포에 발현된 TREK-1 채널에 대한 커큐민, 퀘르세틴, EGCG의 $IC_{50}$는 각각 $1.04{\pm}0.19\;{\mu}M$, $1.13{\pm}0.26\;{\mu}M$, $13.5{\pm}2.20\;{\mu}M$ 이었다. 이러한 결과는 플라보노이드가 TREK-1 채널을 억제하며, 이 조절은 신경계 또는 종양세포에서 플라보노이드의 약리학적 작용 중의 하나임을 제시한다.