Myricetin
(Synonyms: 杨梅素; Cannabiscetin; 杨梅酮) 目录号 : GN10634A potent antioxidant
Cas No.:529-44-2
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Myricetin is a common plant-derived flavonoid with a wide range of activities including strong anti-oxidant, anticancer, antidiabetic and anti-inflammatory activities.
Myricetin exhibits the scavenging activity towards a number of radicals and ions. It displays poor activity (IC50 value=1.4 mg/mL) in a superoxide dismutase (SOD)-like activity assay[1]. It prevents cancer cell death via apoptosis via regulation of PI3K/Akt and MAPK signalling pathways[2]. Myricetin exhibits antiphotoaging effects by quenching causative free radicals in the skin. Myricetin is able to suppress UVB-induced COX-2 expression in mouse skin epidermal JB6 P+ cells. It inhibits UVB-induced initiation of activator protein-1 and NF-κβ, as well as Fyn kinase activity[1]. Myricetin inhibits viability of SKOV3 ovarian cancer cells in a dose-dependent manner. It induces DNA DSBs and ER stress, which leads to apoptosis in SKOV3 cells[3]. Myricetin inhibits human Hsp70 by more than 80% with IC50 values of 83, 11 and 12 μM, respectively[4].
Treatment of orthotopic pancreatic tumors with myricetin results in tumor regression and decreases metastatic spread[2]. Exposure to 150 μM myricetin causes 14%, 26%, 5% and 49% inhibition of rabbit platelet aggregation, induced by ADP, arachidonic acid, collagen and PAF, respectively[5].
References:
[1]. Semwal DK, et al. Myricetin: A Dietary Molecule with Diverse Biological Activities. Nutrients. 2016 Feb 16;8(2):90.
[2]. Phillips PA, et al. Myricetin induces pancreatic cancer cell death via the induction of apoptosis and inhibition of thephosphatidylinositol 3-kinase (PI3K) signaling pathway. Cancer Lett. 2011 Sep 28;308(2):181-8.
[3]. Xu Y, et al. Myricetin induces apoptosis via endoplasmic reticulum stress and DNA double-strand breaks in human ovarian cancer cells. Mol Med Rep. 2016 Mar;13(3):2094-100.
[4]. Jinwal UK, et al. Chemical Manipulation of Hsp70 ATPase Activity Regulates Tau Stability. J Neurosci. 2009 Sep 30;29(39):12079-88.
[5]. Tzeng SH, et al. Inhibition of platelet aggregation by some flavonoids. Thromb Res. 1991 Oct 1;64(1):91-100.
制备储备液 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 3.1423 mL | 15.7114 mL | 31.4228 mL |
5 mM | 0.6285 mL | 3.1423 mL | 6.2846 mL |
10 mM | 0.3142 mL | 1.5711 mL | 3.1423 mL |
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 % saline | ||||||||||
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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 saline,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。
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