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(-)-Epigallocatechin Gallate

抗氧化和表观遗传修饰剂;抑制DNA甲基转移酶(DNM)
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¥1,160.00

产品号 #(选择产品)

产品号 #73642_C

抗氧化和表观遗传修饰剂;抑制DNA甲基转移酶(DNM)

总览

(-)-表没食子儿茶素没食子酸酯是绿茶中含量最丰富的多酚儿茶素抗氧化剂(Frémont et al.; Johnson & Maddipati; Miller & Rice-Evans),能够抑制DNA甲基转移酶(DNMTs;IC₅₀=0.21-0.47 μM;Lee et al.)。(-)-表没食子儿茶素没食子酸酯还能抑制氧化低密度脂蛋白的形成(Yoshida et al.),而氧化低密度脂蛋白在心血管疾病和动脉粥样硬化的病理学中起着重要作用(Itabe et al.)。(-)-表没食子儿茶素没食子酸酯还被证实能够抑制过氧亚硝酸盐介导的8-氧代脱氧鸟苷和3-硝基酪氨酸的形成(Fiala et al.)。

分化
·通过诱导破骨细胞样多核细胞而非成骨细胞的细胞死亡来抑制骨吸收(Nakagawa et al.)。

癌症研究
·抑制小鼠异种移植模型中人胰腺癌细胞的生长并诱导其凋亡(Shankar et al., Du et al.)
·导致人表皮样癌细胞系的细胞周期失调和凋亡,可能是通过抑制NF-κB实现(Ahmad et al.)。

别名
EGCG;NVP-XAA723;茶多酚
 
细胞类型
癌细胞及细胞系,心肌细胞,PSC衍生,成骨细胞
 
种属
人,小鼠,非人灵长类,其他物种,大鼠
 
应用
分化
 
研究领域
癌症,干细胞生物学
 
CAS 编号
989-51-5
 
化学式
C₂₂H₁₈O₁₁
 
分子量
458.4 g/mol
 
纯度
≥98%
 
通路
表观遗传学
 
靶点
DNMT
 

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Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
73644
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
73644
Lot #
All
Language
English

应用领域

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相关材料与文献

文献 (11)

文献 (11)

Antioxidant activity of resveratrol and alcohol-free wine polyphenols related to LDL oxidation and polyunsaturated fatty acids. Fré et al. Life sciences 1999 JAN

Abstract

Wine polyphenols were examined for their capacity to protect the lipid and protein moieties of porcine low density lipoproteins (LDL) during oxidation. The efficiency of resveratrol (3,4',5,trihydroxystilbene) and defined flavonoids was compared to that of a wine extract (WE) containing 0.5 g/g proanthocyanidols. The efficiency of resveratrol for protecting polyunsaturated fatty acids (PUFA) was higher than that of flavonoids in copper-induced oxidation and lower in AAPH (radical initiator)-induced oxidation. The LDL receptor activity was evaluated by flow cytometry using LDL labeled with fluorescein isothiocyanate (FITC) and Chinese hamster ovary cells (CHO-K1). The incubation of CHO-K1 with FITC-LDL oxidized for 16 h reduced the proportion of fluorescent cells from 97% to 4%. At a concentration of 40 microM,resveratrol and flavonoids completely restored the uptake of copper-oxidized LDL and AAPH-oxidized LDL respectively. Total fluorescence could also be obtained with 20 mg/L of WE with both oxidation systems. These data are consistent with previous findings relative to the formation of degradative products from PUFA. They confirm that resveratrol was more effective than flavonoids as a chelator of copper and less effective as a free-radical scavenger. Moreover,they show that WE,which contained monomeric and oligomeric forms of flavonoids and phenolic acids,protected LDL by both mechanisms.
Inhibitory effect of tea flavonoids on the ability of cells to oxidize low density lipoprotein. Yoshida H et al. Biochemical pharmacology 1999 DEC

Abstract

Dietary flavonoid intake has been reported to be inversely related to mortality from coronary heart disease,and the anti-atherosclerotic effect of flavonoids is considered to be due probably to their antioxidant properties. Oxidation of low density lipoprotein (LDL) has been reported to be induced by the constituent cells of the arterial wall. Accordingly,we examined the effect of pretreatment with tea flavonoids,such as theaflavin digallate,on the ability of cells to oxidize LDL. Theaflavin digallate pretreatment of macrophages or endothelial cells reduced cell-mediated LDL oxidation in a concentration- (0-400 microM) and time- (0-4 hr) dependent manner. This inhibitory effect of flavonoids on cell-mediated LDL oxidation was in the order of theaflavin digallate textgreater theaflavin textgreater or = epigallocatechin gallate textgreater epigallocatechin textgreater gallic acid. Further,we investigated the mechanisms by which flavonoids inhibited cell-mediated LDL oxidation using macrophages and theaflavin digallate. Theaflavin digallate pretreatment decreased superoxide production of macrophages and chelated iron ions significantly. These results suggest that tea flavonoids attenuate the ability of the cell to oxidize LDL,probably by reducing superoxide production in cells and chelating iron ions.
Green tea polyphenol epigallocatechin-3-gallate differentially modulates nuclear factor kappaB in cancer cells versus normal cells. Ahmad N et al. Archives of biochemistry and biophysics 2000 APR

Abstract

Green tea has shown remarkable anti-inflammatory and cancer chemopreventive effects in many animal tumor bioassays,cell culture systems,and epidemiological studies. Many of these biological effects of green tea are mediated by epigallocatechin 3-gallate (EGCG),the major polyphenol present therein. We have earlier shown that EGCG treatment results in apoptosis of several cancer cells,but not of normal cells (J. Natl. Cancer Inst. 89,1881-1886 (1997)). The mechanism of this differential response of EGCG is not known. In this study,we investigated the involvement of NF-kappaB during these differential responses of EGCG. EGCG treatment resulted in a dose-dependent (i) inhibition of cell growth,(ii) G0/G1-phase arrest of the cell cycle,and (iii) induction of apoptosis in human epidermoid carcinoma (A431) cells,but not in normal human epidermal keratinocytes (NHEK). Electromobility shift assay revealed that EGCG (10-80 microM) treatment results in lowering of NF-kappaB levels in both the cytoplasm and nucleus in a dose-dependent manner in both A431 cells and NHEK,albeit at different concentrations. EGCG treatment was found to result in a dose-based differential inhibition of TNF-alpha- and LPS-mediated activation of NF-kappaB in these cells. The inhibition of NF-kappaB constitutive expression and activation in NHEK was observed only at high concentrations. The immunoblot analysis also demonstrated a similar pattern of inhibition of the constitutive expression as well as activation of NF-kappaB/p65 nuclear protein. This inhibition of TNF-alpha-caused NF-kappaB activation was mediated via the phosphorylative degradation of its inhibitory protein IkappaBalpha. Taken together,EGCG was found to impart differential dose-based NF-kappaB inhibitory response in cancer cells vs normal cells; i.e.,EGCG-mediated inhibition of NF-kappaB constitutive expression and activation was found to occur at much higher dose of EGCG in NHEK as compared to A431 cells. This study suggests that EGCG-caused cell cycle deregulation and apoptosis of cancer cells may be mediated through NF-kappaB inhibition.

更多信息

更多信息
Molecular Weight 458.4 g/mol
物种 人, 其它物种, 大鼠, 小鼠, 非人灵长类
Alternative Names EGCG; NVP-XAA723; Tea catechin
Cas Number 989-51-5
Chemical Formula C₂₂H₁₈O₁₁
纯度 ≥ 98%
Target DNMT
Pathway Epigenetic
质量保证:

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