970-74-1
970-74-1 結(jié)構(gòu)式
基本信息
綠茶兒茶酚
表沒食子兒茶素
(-)-表沒食子酸兒茶素
表沒食子兒茶素 (EGC)
(EGC) 表沒食子酸兒茶素
L-表沒食子兒茶精
(-)-表沒食子兒茶素
(2R,3R)-2-(3,4,5-TRIHYDROXYPHENYL)-3,4-DIHYDRO-1(2H)-BENZOPYRAN-3,5,7-TRIOL
3,3',4',5,5',7-HEXAHYDROXYFLAVAN
(-)-3,5,7,3',4',5'-HEXAHYDROXYLFLAVAN
(-)-CIS-2-(3,4,5-TRIHYDROXYPHENYL)-3,4-DIHYDRO-1(2H)-BENZOPYRAN-3,5,7-TRIOL
(-)-CIS-3,3',4',5,5',7-HEXAHYDROXYFLAVANE
(-)-EGC
(-)-EPIGALLOCATECHIN
EPIGALLOCATECHIN
EPIGALLOCATECHIN,(-)-
(-)-epigallocatechol
3,3’,4’,5,5’,7-flavanhexol
5,7-triol,3,4-dihydro-2-(3,4,5-trihydroxyphenyl)-2h-1-benzopyran-(2r-cis
antiscurvyfactorc(sub2)
epigallocatechol
Greenteacatechins
l-epigallocatechin
(−
)-Epigallocatechin
EPIGALLOCATECHIN (EGC) FROM GREEN TEA 70% BY HPLC
EPIGALLOCATECHIN (EGC) FROM GREEN TEA 50% BY HPLC
物理化學(xué)性質(zhì)
安全數(shù)據(jù)
常見問題列表
(-)-表沒食子兒茶素用于分析含量鑒定/測定，藥理活性篩選；
表沒食子兒茶素具有如下生理作用：
1，表沒食子兒茶素具有抗氧化作用，能夠保護(hù)生物膜免受自由基誘導(dǎo)的氧化性損傷。
2，表沒食子兒茶素具有降血脂作用，能預(yù)防動(dòng)脈粥樣硬化和心血管疾病等多種生物學(xué)功能，甚至認(rèn)為比維生素E強(qiáng)。
3，表沒食子兒茶素具有抗癌活性，活性比表沒食子兒茶素沒食子酸酯略低。
(-)-Epigallocatechin (EGC) is a potent inhibitor of amyloidogenic cystatin I66Q amyloid fibril formation in vitro. Computational analysis suggests that (-)-Epigallocatechin prevents amyloidogenic cystatin fibril formation by stabilizing the molecule in its native-like state as opposed to redirecting aggregation to disordered, amorphous aggregates [1]. Combined curcumin and EGCG treatment reduced the cancer stem-like Cluster of differentiation 44 (CD44)-positive cell population. Western blot and immunoprecipitation analyses revealed that curcumin and (-)-Epigallocatechin (EGC) specifically inhibited STAT3 phosphorylation and STAT3-NFkB interaction was retained [2]. (-)-Epigallocatechin (EGC) exhibits a MIC and MBC of 5 μg/mL and 20 μg/mL respectively and effectively eradicated E. faecalis biofilms. (-)-Epigallocatechin induces the formation of hydroxyl radicals in E. faecalis. The addition of DIP protected E. faecalis against EGCG-mediated antibacterial effects. At sub-MIC, (-)-Epigallocatechin induces significant down-regulation of E. faecalis virulence genes [3].