您好,欢迎来到化工原料网! [登录] [免费注册]
化工原料网
位置:首页 > 产品库 > Resveratrol
立即咨询
咨询类型:
     
*姓名:
*电话:
*单位:
Email:
*留言内容:
请详细说明您的需求。
*验证码:
 
Resveratrol
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Resveratrol图片
包装与价格:
包装价格(元)
10mM (in 1mL DMSO)电议
200mg电议
500mg电议

产品介绍

Cell lines

ALVA-41, PC-3, and BPH-1 cells

Preparation Method

For cell viability studies, ALVA-41, PC-3, and BPH-1 cells were treated for 24 h with 10 µmol/L and 100 µmol/L concentrations of resveratrol or EGCG.

Reaction Conditions

10, 100 µM for 24 hours

Applications

Resveratrol at low doses (10 µmol/L) induced a proliferative response in ALVA-41 and BPH-1 cells at 24 h, which was not evident in PC-3 cells. However, at a higher dose (100 µmol/L), resveratrol produced a significant toxicity in prostate cancer cells, although the effect on ALVA-41 cells was relatively greater than on PC-3 cells.

Animal models

CB17SC mice model injected with LAPC-4 cells

Preparation Method

In the primary LAPC-4 study, mice were fed no resveratrol (control), 50 mg/kg/day resveratrol (RV50), or 100 mg/kg/day resveratrol (RV100).

Dosage form

Fed in diet, 50 mg/kg/day and 100 mg/kg/day

Applications

In the LAPC-4 study, RV50 significantly decreased survival while RV100 did not significantly change survival.

产品描述

Resveratrol (trans-Resveratrol; SRT501) is a phytoalexin. Resveratrol is a potent reducing agent, and can prevent carcinogenesis due to its anti-oxidant abilities[1]. Resveratrol has a broad range of targets, including cyclooxygenase (e.g., COX, IC50=1.1 μM), lipoxygenase (LOC, IC50=2.7 μM), STAT3 (IC50=20 μM), and other proteins[2,3].

Resveratrol treatment is found to exert its effect on renal cell carcinoma (RCC) proliferation, migration and invasion in a concentration dependent manner through inactivation of the Akt and ERK1/2 signaling pathways[4]. In CaCo-2 cells, treatment with 25 μM Resveratrol has shown 70% growth inhibition due to S/G2 phase arrest[5]. Resveratrol treatment lead to inhibited invasion and metastasis of colorectal cancer-derived cell lines LoVo and HCT116 by suppressing the Wnt/β-catenin signaling mediated target genes of c-Myc, MMP-7, and MALT-1[6].

Resveratrol is shown to be effective against breast cancer metastasis to lungs in mice by its inhibitory effect on Stat3 mediated signaling[7]. Resveratrol treatment reduced size and number of tumor spheres in renal carcinoma stem cells xenograft mice model [8]. Resveratrol treatment reduced Epithelial to mesenchymal transition (EMT) of glioblastoma U87 xenografted mice models[9].

References:
[1]. Bhaskara V K, Mittal B, Mysorekar V V, et al. Resveratrol, cancer and cancer stem cells: A review on past to future[J]. Current Research in Food Science, 2020, 3: 284-295.
[2]. Calamini B, Ratia K, Malkowski M G, et al. Pleiotropic mechanisms facilitated by resveratrol and its metabolites[J]. Biochemical Journal, 2010, 429(2): 273-282.
[3]. Pirola L, FrOjdO S. Resveratrol: one molecule, many targets[J]. IUBMB life, 2008, 60(5): 323-332.
[4]. Zhao Y, Tang H, Zeng X, et al. Resveratrol inhibits proliferation, migration and invasion via Akt and ERK1/2 signaling pathways in renal cell carcinoma cells[J]. Biomedicine & Pharmacotherapy, 2018, 98: 36-44.
[5]. Schneider Y, Vincent F, Duranton B, et al. Anti-proliferative effect of resveratrol, a natural component of grapes and wine, on human colonic cancer cells[J]. Cancer letters, 2000, 158(1): 85-91.
[6]. Ji Q, Liu X, Fu X, et al. Resveratrol inhibits invasion and metastasis of colorectal cancer cells via MALAT1 mediated Wnt/β-catenin signal pathway[J]. PloS one, 2013, 8(11): e78700.
[7]. Lee-Chang C, Bodogai M, Martin-Montalvo A, et al. Inhibition of breast cancer metastasis by resveratrol-mediated inactivation of tumor-evoked regulatory B cells[J]. The Journal of Immunology, 2013, 191(8): 4141-4151.
[8]. Ji Q, Liu X, Fu X, et al. Resveratrol inhibits invasion and metastasis of colorectal cancer cells via MALAT1 mediated Wnt/β-catenin signal pathway[J]. PloS one, 2013, 8(11): e78700.
[9]. Song Y, Chen Y, Li Y, et al. Resveratrol suppresses epithelial-mesenchymal transition in GBM by regulating Smad-dependent signaling[J]. BioMed Research International, 2019, 2019.