Calycosin-7-O-β-D-glucoside is an isoflavone isolated from Astragali Radix. Calycosin-7-O-β-D-glucoside has variety of biological activities, such as neuroprotective, cardioprotection, anti-inflammation, and antioxidative stress effects[1][2].
体外研究 (In Vitro)
Calycosin-7-O-β-D-glucoside (2 μM; 6 hours) remarkably inhibits the expression and activities of MMPs, and secures the expression of cav-1 and tight junction proteins in the microvessels isolated from ischemic rat cortex[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Calycosin-7-O-β-D-glucoside (intraperitoneal injection; 26.8 mg/kg; 14 days) significantly reduces infarct volume, histological damage and BBB permeability in the in vivo MCAO ischemia-reperfusion rat model[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Middle cerebral artery occlusion (MCAO) male adult Sprague-Daweley rats[1]
Dosage:
26.8 mg/kg
Administration:
Intraperitoneal injection; 26.8 mg/kg; 14 days
Result:
Exhibited neuroprotective effects in rats.
分子量
446.40
Formula
C22H22O10
CAS 号
20633-67-4
中文名称
毛蕊异黄酮苷;毛蕊异黄酮苷;毛蕊异黄酮-7-O-β-D 葡萄糖苷
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Shuping Fu, et al. Calycosin-7-O-β-D-glucoside regulates nitric oxide /caveolin-1/matrix metalloproteinases pathway and protects blood-brain barrier integrity in experimental cerebral ischemia-reperfusion injury. J Ethnopharmacol. 2014 Aug 8;155(1):692-701.
[2]. Xiangli Yan, et al. Calycosin-7- O- β- D-glucoside Attenuates OGD/R-Induced Damage by Preventing Oxidative Stress and Neuronal Apoptosis via the SIRT1/FOXO1/PGC-1 α Pathway in HT22 Cells. Neural Plast. 2019 Dec 1;2019:8798069.
Calycosin (Cyclosin) is a natural active compound with anti-oxidative and anti-inflammation activity. IC50 value: Target: in vitro: calycosin had obvious anti-proliferation effects on SKOV3 cells in a dose- and time-dependent manner. calycosin up-regulated the Bax/Bcl-2 ratio and cleaved caspase-3, cleaved caspase-9 expression in a dose-dependent manner. In summary, calycosin might exert anti-growth and induce-apoptosis activity against ovarian cancer SKOV3 cells through activating caspases and Bcl-2 family proteins, therefore presenting as a promising therapeutic agent for the treatment of ovarian cancer [1]. Both calycosin and genistein inhibited proliferation and induced apoptosis in MCF-7 breast cancer cells, especially after treatment with calycosin. Treatment of MCF-7 cells with calycosin or genistein resulted in decreased phosphorylation of Akt, and decreased expression of its downstream target, HOTAIR [2]. incubation of calycosin resulted in enhanced expression ERβ in MCF-7 and T-47D cells, rather than MDA-231 and MDA-435 cells. Moreover, with the upregulation of ERβ, successive changes in downstream signaling pathways were found, including inactivation of insulin-like growth factor 1 receptor (IGF-1R), then stimulation of p38 MAPK and suppression of the serine/threonine kinase (Akt), and finally poly(ADP-ribose) polymerase 1 (PARP-1) cleavage [3]. in vivo: calycosin stimulated a dramatic increase in uterine weight and downregulated the level of ERα protein in OVX mice [4].
分子量
284.26
Formula
C16H12O5
CAS 号
20575-57-9
中文名称
毛蕊异黄酮;异黄酮
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Zhou Y, et al. Calycosin induces apoptosis in human ovarian cancer SKOV3 cells by activating caspases and Bcl-2 family proteins. Tumour Biol. 2015 Feb 12.
[2]. Chen J, et al. Calycosin and genistein induce apoptosis by inactivation of HOTAIR/p-Akt signaling pathway in human breast cancer MCF-7 cells. Cell Physiol Biochem. 2015;35(2):722-8.
[3]. Chen J, et al. Calycosin suppresses breast cancer cell growth via ERβ-dependent regulation of IGF-1R, p38 MAPK and PI3K/Akt pathways. PLoS One. 2014 Mar 11;9(3):e91245.
[4]. Chen J, et al. Calycosin promotes proliferation of estrogen receptor-positive cells via estrogen receptors and ERK1/2 activation in vitro and in vivo. Cancer Lett. 2011 Sep 28;308(2):144-51.