(-)-Epigallocatechin gallate (EGCG) |
| 目录号 GC14049 |
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
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Purity: >99.50%
- COA (Certificate Of Analysis)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
Human and rat neural progenitor cells (NPCs) |
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Preparation method |
The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
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Reaction Conditions |
0, 1, 2, 5 and 10 μM; 24 or 48 hrs |
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Applications |
(-)-Epigallocatechin Gallate (EGCG) altered human and rat NPC development in vitro. EGCG affected migration distance, migration pattern and nuclear density of NPCs growing as neurospheres. EGCG exerted these functional impairments by binding to the extracellular matrix (ECM) glycoprotein laminin, preventing its binding to β1-integrin subunits, thereby prohibiting cell adhesion and resulting in altered glia alignment and decreased number of migrating young neurons. |
| Animal experiment [2]: | |
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Animal models |
A rat model of partial bladder outlet obstruction (pBOO)-induced bladder injury |
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Dosage form |
4.5 mg/kg/day; i.p.; 2 days or 30 days |
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Applications |
EGCG attenuated bladder inflammation caused by pBOO at the 48th hr. At the 30th day, EGCG attenuated endoplasmic reticulum (ER) stress-related apoptosis. In addition, EGCG improved bladder compliance, contractile frequency and inflammation at the 30th day. |
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Other notes |
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
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References: [1]. Barenys M, Gassmann K, Baksmeier C, Heinz S, Reverte I, Schmuck M, Temme T, Bendt F, Zschauer TC, Rockel TD, Unfried K, W?tjen W, Sundaram SM, Heuer H, Colomina MT, Fritsche E. Epigallocatechin gallate (EGCG) inhibits adhesion and migration of neural progenitor cells in vitro. Arch Toxicol. 2016 Apr 26. [2]. Hsieh JT, Kuo KL, Liu SH, Shi CS, Chang HC, Lin WC, Chou CT, Hsu CH, Liao SM, Wang ZH, Li CC, Huang KH. Epigallocatechin Gallate Attenuates Partial Bladder Outlet Obstruction-induced Bladder Injury via Suppression of Endoplasmic Reticulum Stress-related Apoptosis-In Vivo Study. Urology. 2016 May;91:242.e1-9. |
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(-)-表没食子儿茶素没食子酸酯 (EGCG) 是一种主要的儿茶素，占绿茶中儿茶素总量的 59%，是一种强大的抗氧化剂以及抗血管生成和抗肿瘤剂。EGCG 已被研究用于化学预防多种癌症，包括肝癌、胃癌、皮肤癌、肺癌、乳腺癌和结肠癌。研究结果表明，EGCG能够通过影响信号转导途径诱导细胞凋亡、促进细胞生长停滞和阻断致癌作用。此外，EGCG 对多种病毒具有抑制作用，包括 HCV、HIV-1、HBV、HSV-1、HSV-2、EBV、腺病毒、流感病毒和肠道病毒，以及多种酶，包括 DNMT、蛋白酶和 DHFR。
参考
Singh BN、Shankar S、Srivastava RK。绿茶儿茶素，表没食子儿茶素-3-没食子酸酯（EGCG）：机制、前景和临床应用。生化药理学。2011年；82（12）：1807-1821。
Steinmann J、Buer J、Pietschmann T、Steinmann E. 绿茶的一种成分表没食子儿茶素 3-没食子酸酯 (EGCG) 的抗感染特性。Br J Pharmacol。2013年；168(5):1059-1073
| Cas No. | 989-51-5 | SDF | |
| 别名 | EGCG | ||
| 化学名 | [(2R,3R)-5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)-3,4-dihydro-2H-chromen-3-yl] 3,4,5-trihydroxybenzoate | ||
| Canonical SMILES | C1C(C(OC2=CC(=CC(=C21)O)O)C3=CC(=C(C(=C3)O)O)O)OC(=O)C4=CC(=C(C(=C4)O)O)O | ||
| 分子式 | C22H18O11 | 分子量 | 458.37 |
| 溶解度 | ≥ 22.9mg/mL in DMSO; ≥ 20mg/mL in Water | 储存条件 | Store at -20°C |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. | ||
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
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| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % ddH2O | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL ddH2O，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Abstract
EGCG prevents cardiac mitochondrial metabolism and apoptosis in CS-exposed rats and exhibits enduring cardio protection at mitochondrial level, where it shelters the activities of TCA cycle enzymes and antioxidant enzymes from CS exposure with concomitant decrease in lipid peroxidation and increase in GSH level, inhibits apoptosis through a series of cellular events, including inhibition of the release of cytochrome c into cytosol, activation of pro-caspase-3, down-regulation of Bax and up-regulation of Bcl-2, and reverses the ultra structural apoptotic alternations of mitochondria and nucleus.
Abstract
EGCG, which causes positive results in in vitro mammalian genotoxicity assays via oxidative stress and negative results in in vivo MN studies, was used to assess the effect of cell differentiation status on MN induction and significantly induced the expression of genotoxic response related genes in NHEKs after 12h. The Oxidative stress probably caused by EGCG can be eliminated by EpiDermTM under in vitro experimental conditions.
Abstract
EGCG, a strong antioxidant with possible anti-obesity and anti-diabetic effects, was administered intraperitoneally to alloxan-induced diabetic mice at doses of 50mg/kg body weight for a period of 7 days resulting in a significant increase of body weight and haematological/immunological blood parameters, 100% survival, a significant decrease of lipid peroxidation in liver, kidney and brain tissue, and remarkably reduced DNA damage in peripheral lymphocytes. Due to the demonstrated beneficial effects against diabetes and the associated consequences of free-radical formation in kidney, liver, spleen and brain tissues, EGCG could be used as a dietary supplement potentially contributing to nutritional strategies for the prevention and treatment of diabetes mellitus.
Abstract
EGCG is involved in UVB irradiation-induced autophagy in RPE cells, where the treatment of EGCG significantly reduced the formation of LC3-II and autohagosomes and remarkably relieved UVB irradiation-induced toxicity to RPE cells in an autophagy-dependent manner, and is a potential therapeutic reagent that could be incorporated into the treatment of pathological conditions associated with abnormal autophagy.
Abstract
EGCG, which is hepatotoxic to humans and animals, barely affected oxidative phosphorylation at 7.5-100 μΜ in normal mitochondria of rats liver but remarkably inhibited RCCs in mitochondria undergoing Ca(2+) overload-induced MPT only if IM integrity was compromised. EGCG promotes Ca(2+) overload-induced MPT after moderate MPT has already commenced and worsens pre-existing mitochondria abnormalities triggering hepatotoxicity since it only targets hepatic RCCs in swelling mitochondrial other than normal mitochondrial.