CAS NO: | 491-54-3 |
规格: | 98% |
分子量: | 300.26 |
包装 | 价格(元) |
5mg | 询价 |
10mg | 询价 |
50mg | 询价 |
Background:
The effects of phytoestrogens have been studied in the hypothalamic-pituitary-gonadal axis and various non-gonadal targets. Epidemiologic and experimental evidence indicates a protective effect of phytoestrogens also in colorectal cancer. The mechanism through which estrogenic molecules control colorectal cancer tumorigenesis could possibly involve estrogen receptor β, which is the predominantly expressed estrogen receptor subtype in colon mucosa.
In vitro: Kaempferide triglycoside proved to inhibit the proliferation of native and estrogen receptor β overexpressing colon cancer cells via a mechanism not mediated by ligand binding dependent estrogen receptor activation. It affected HCT8 cell cycle progression through increasing the G0/G1 cell fraction and in estrogen receptor β overexpressing cells increased two antioxidant enzymes [1].
In vivo: The aim of one previous study was to evaluate the effect of kaempferol on tissue lipid peroxidation and antioxidant status in 1,2-dimethyl hydrazine induced colorectal cancer in male Wistar rats and to compare its efficacy with irinotecan. This study revealed that kaempferol could be safely used as a chemopreventive agent in colorectal cancer [2].
Clinical trial: Up to now, kaempferide is still in the preclinical development stage.
Reference:
[1] Martineti V, Tognarini I, Azzari C, Carbonell Sala S, Clematis F, Dolci M, Lanzotti V, Tonelli F, Brandi ML, Curir P. Inhibition of in vitro growth and arrest in the G0/G1 phase of HCT8 line human colon cancer cells by kaempferide triglycoside from Dianthus caryophyllus. Phytother Res. 2010 Sep;24(9):1302-8.
[2] Nirmala P, Ramanathan M. Effect of kaempferol on lipid peroxidation and antioxidant status in 1,2-dimethyl hydrazine induced colorectal carcinoma in rats. Eur J Pharmacol. 2011 Mar 1;654(1):75-9.
维奥蛋白资源库 - 中文蛋白资源 CopyRight © 2010-2024 |