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Calycosin Sale

(Synonyms: 异黄酮; Cyclosin) 目录号 : GN10667

An isoflavone with diverse biological activities

Calycosin Chemical Structure

Cas No.:20575-57-9

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20mg
¥1,869.00
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实验参考方法

Cell experiment [1]:

Cell lines

MCF-7 and T47D cells

Preparation Method

MCF-7 and T47D cells were cultured and treated in triplicate with various doses (0, 6.25, 12.5, 25, 50, 100 and 150 µM) of calycosin for 48 h.

Reaction Conditions

0- 150 µM calycosin for 48 h

Applications

Treatment with Calycosin lower doses (6.25 or 12.5 µM) promoted proliferation of breast cancer cells, but with higher doses significantly reduced the viability of MCF-7 and T47D cells.

Animal experiment [2]:

Animal models

MG-63 tumor-bearing nude mice(eight weeks-of-age, weighing between 17-22 g)

Preparation Method

Ten days after implantation of the GM-63 cells, when tumors were seen to develop, mice were randomly divided into five groups: a control group, an ifosfamide-treated group (4mg/kg), and three calycosin-treated groups (2, 4, and 8 mg/kg)treated by intraperitoneal injection. Calycosin and ifosfamide were injected daily for 15 days.

Dosage form

2, 4, and 8 mg/kg calycosin for 15 days

Applications

In the nude mouse MG-63 tumor xenografts, calycosin inhibited tumor growth and regulated the expression levels of apoptosis-related PI3K/AKT/mTOR pathway proteins.

References:

[1]. Li S, Wang Y, et,al. Calycosin Inhibits the Migration and Invasion of Human Breast Cancer Cells by Down-Regulation of Foxp3 Expression. Cell Physiol Biochem. 2017;44(5):1775-1784. doi: 10.1159/000485784. Epub 2017 Dec 6. PMID: 29241196.
[2]. Sun H, Yin M,et,al. Calycosin, a Phytoestrogen Isoflavone, Induces Apoptosis of Estrogen Receptor-Positive MG-63 Osteosarcoma Cells via the Phosphatidylinositol 3-Kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Pathway. Med Sci Monit. 2018 Sep 5;24:6178-6186. doi: 10.12659/MSM.910201. PMID: 30182951; PMCID: PMC6134888.

产品描述

Calycosin (CA, 7, 3-dihydroxy-4-methoxy isoflavone, C16H12O5) is one of the flavonoids extracted from astragalus root, also known as the typical phytoestrogens[1,2]. Calycosin is widely used in the pharmaceutical and food fields, and likely to be taken at low or high doses in daily life[3].

Treatment with Calycosin lower doses (6.25 or 12.5 μM) promoted proliferation of breast cancer cells, but with higher doses significantly reduced the viability of MCF-7 and T47D cells. Furthermore, higher doses of calycosin were found to inhibit migration and invasion of the two cell lines in a dose-dependent manner[4]. Calycosin induced apoptosis of osteosarcoma cells (143B) via increasing caspase-3 protein levels, reducing intracellular Bcl-2B-cell lymphoma 2 (Bcl-2) protein expression and up-regulating apoptotic protease activating factor-1 (Apaf-1) in tumors[5]. Moreover, Calycosin induced apoptosis of osteosarcoma cells through the dose-dependent reducing proliferating cell nuclear antigen and the expression of Bcl-2, and increasing the cleavage of Poly (ADP-ribose) polymerase (PARP)[7]. Calycosin also has antioxidant properties (SC50 = 42.53±1.77 μg/mL)[9].

In estrogen receptor (ER)-positive MG-63 human osteosarcoma cells and MG-63 tumor-bearing nude mice, Calycosin induced apoptosis of osteosarcoma cells by increasing the expression of the phosphorylated-phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR pathway proteins[6]. Calycosin can play an anti-inflammatory role by binding with IL-6. Calycosin inhibited kidney inflammation caused by diabetes by inhibiting the phosphorylation of IκBα and nuclear factor κB (NF-κB)/p65 in vitro and in vivo[8].

References:
[1]. Deng M, Chen H,et,al. Calycosin: a Review of its Pharmacological Effects and Application Prospects. Expert Rev Anti Infect Ther. 2021 Jul;19(7):911-925. doi: 10.1080/14787210.2021.1863145. Epub 2020 Dec 21. PMID: 33346681.
[2]. Wang, Yl., Liang, Yz., et,al. Simultaneous separation and determination of four main isoflavonoids in Astragali Radix by an isocratic LC/ESI-MS method. J. Cent. South Univ. 23, 303-309 (2016). https://doi.org/10.1007/s11771-016-3074-4
[3]. Zhang LJ, Liu HK, et,al. New isoflavonoid glycosides and related constituents from astragali radix ( Astragalus membranaceus ) and their inhibitory activity on nitric oxide production. J Agric Food Chem. 2011 Feb 23;59(4):1131-7. doi: 10.1021/jf103610j. Epub 2011 Jan 31. PMID: 21280630.
[4]. Li S, Wang Y, et,al. Calycosin Inhibits the Migration and Invasion of Human Breast Cancer Cells by Down-Regulation of Foxp3 Expression. Cell Physiol Biochem. 2017;44(5):1775-1784. doi: 10.1159/000485784. Epub 2017 Dec 6. PMID: 29241196.
[5]. Qiu R, Ma G, et,al.Antineoplastic effect of calycosin on osteosarcoma through inducing apoptosis showing in vitro and in vivo investigations. Exp Mol Pathol. 2014 Aug;97(1):17-22. doi: 10.1016/j.yexmp.2014.04.014. Epub 2014 May 4. PMID: 24797937.
[6]. Sun H, Yin M, et,al. Calycosin, a Phytoestrogen Isoflavone, Induces Apoptosis of Estrogen Receptor-Positive MG-63 Osteosarcoma Cells via the Phosphatidylinositol 3-Kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Pathway. Med Sci Monit. 2018 Sep 5;24:6178-6186. doi: 10.12659/MSM.910201. PMID: 30182951; PMCID: PMC6134888.
[7]. Qiu R, Ma G, et,al.Clinical case report of patients with osteosarcoma and anticancer benefit of calycosin against human osteosarcoma cells. J Cell Biochem. 2019 Jun;120(6):10697-10706. doi: 10.1002/jcb.28360. Epub 2019 Jan 16. PMID: 30652346.
[8]. Elsherbiny NM, Said E, et,al. Renoprotective effect of calycosin in high fat diet-fed/STZ injected rats: Effect on IL-33/ST2 signaling, oxidative stress and fibrosis suppression. Chem Biol Interact. 2020 Jan 5;315:108897. doi: 10.1016/j.cbi.2019.108897. Epub 2019 Nov 11. PMID: 31726037.
[9].Toukam, Paul Djouonzo, et al. "Novel saponin and benzofuran isoflavonoid with in vitro anti-inflammatory and free radical scavenging activities from the stem bark of Pterocarpus erinaceus (Poir)." Phytochemistry Letters (2018): n. pag.

毛蕊花素(CA, 7, 3-dihydroxy-4-methoxy isflavone, C16H12O5)是从黄芪中提取的黄酮类化合物之一,也被称为典型的植物雌激素[1,2]。毛蕊花素广泛应用于制药和食品领域,日常生活中可能会以低剂量或高剂量服用[3]。

用较低剂量(6.25 或 12.5 μM)的 Calycosin 治疗可促进乳腺癌细胞的增殖,但较高剂量会显着降低 MCF-7 和 T47D 细胞的活力。此外,发现较高剂量的毛蕊花素以剂量依赖性方式抑制两种细胞系的迁移和侵袭[4]。毛蕊花素通过增加 caspase-3 蛋白水平、降低细胞内 Bcl-2B 细胞淋巴瘤 2 (Bcl-2) 蛋白表达和上调肿瘤中凋亡蛋白酶激活因子-1 (Apaf-1) 诱导骨肉瘤细胞凋亡 (143B) [5].此外,毛蕊花素通过剂量依赖性降低增殖细胞核抗原和 Bcl-2 的表达,并增加聚(ADP-核糖)聚合酶(PARP)的裂解,诱导骨肉瘤细胞凋亡[7]。毛蕊花素还具有抗氧化特性 (SC50 = 42.53±1.77 μg/mL)[9]。

在雌激素受体 (ER) 阳性 MG-63 人骨肉瘤细胞和 MG-63 荷瘤裸鼠中,毛蕊花素通过增加磷酸化磷脂酰肌醇 3-激酶 (PI3K)/Akt 的表达诱导骨肉瘤细胞凋亡/mTOR 通路蛋白[6]。 Calycosin可通过与IL-6结合发挥抗炎作用。毛蕊花素在体内外通过抑制IκBα和核因子κB(NF-κB)/p65的磷酸化来抑制糖尿病引起的肾脏炎症[8]。

Chemical Properties

Cas No. 20575-57-9 SDF
别名 异黄酮; Cyclosin
化学名 7-hydroxy-3-(3-hydroxy-4-methoxyphenyl)chromen-4-one
Canonical SMILES COC1=C(C=C(C=C1)C2=COC3=C(C2=O)C=CC(=C3)O)O
分子式 C16H12O5 分子量 284.26
溶解度 DMSO : ≥ 100 mg/mL (351.79 mM) 储存条件 Store at 2-8°C
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1 mM 3.5179 mL 17.5895 mL 35.1791 mL
5 mM 0.7036 mL 3.5179 mL 7.0358 mL
10 mM 0.3518 mL 1.759 mL 3.5179 mL
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Research Update

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.PMID: 3188553710.1155/2019/8798069

Neuronal apoptosis induced by oxidative stress is a major pathological process that occurs after cerebral ischemia-reperfusion. Calycosin-7-O-β-D-glucoside (CG) is a representative component of isoflavones in Radix Astragali (RA). Previous studies have shown that CG has potential neuroprotective effects. However, whether CG alleviates neuronal apoptosis through antioxidant stress after ischemia-reperfusion remains unknown. To investigate the positive effects of CG on oxidative stress and apoptosis of neurons, we simulated the ischemia-reperfusion process in vitro using an immortalized hippocampal neuron cell line (HT22) and oxygen-glucose deprivation/reperfusion (OGD/R) model. CG significantly improved cell viability and reduced oxidative stress and neuronal apoptosis. In addition, CG treatment upregulated the expression of SIRT1, FOXO1, PGC-1α, and Bcl-2 and downregulated the expression of Bax. In summary, our findings indicate that CG alleviates OGD/R-induced damage via the SIRT1/FOXO1/PGC-1α signaling pathway. Thus, CG maybe a promising therapeutic candidate for brain injury associated with ischemic stroke.

Calycosin: a Review of its Pharmacological Effects and Application Prospects

Expert Rev Anti Infect Ther.2021 Jul;19(7):911-925.PMID: 3334668110.1080/14787210.2021.1863145

Introduction: Calycosin (CA), a typical phytoestrogen extracted from root of Astragalus membranaceus. On the basis of summarizing the pharmacological and pharmacokinetic studies of CA in recent years, we hope to provide useful information for CA about treating different diseases and to make suggestions for future research.Areas covered: We collected relevant information (January 2014 to March 2020) on CA via the Internet database. Keywords searched includ pharmacology, pharmacokinetics and toxicology, and the number of effective references was 118. CA is a phytoestrogen with wide range of pharmacological activities. By affecting PI3K/Akt/mTOR, WDR7-7-GPR30, Rab27B-β-catenin-VEGF, etc. signaling pathway, CA showed the effect of anticancer, anti-inflammatory, anti-osteoporosis, neuroprotection, hepatoprotection, etc. Therefore, CA is prospective to be used in the treatment of many diseases.Expert opinion: Research shows that CA has a therapeutic effect on a variety of diseases. We think CA is a promising natural medicine. Therefore, we propose that the research directions of CA in the future include the following. Carrying out clinical research trials in order to find the most suitable medicinal concentration for different diseases; Exploring the synergistic mechanism of CA in combination with other drugs; Exploring ways to increase the blood circulation concentration of CA.

Calycosin inhibits breast cancer cell migration and invasion by suppressing EMT via BATF/TGF-β1

Aging (Albany NY).2021 Jun 7;13(12):16009-16023.PMID: 34096887DOI: 10.18632/aging.203093

In this study, we investigated the effects of Calycosin on breast cancer cell progression and their underlying mechanisms. Calycosin dose- and time-dependently inhibited proliferation, migration, and invasion by T47D and MCF-7 breast cancer cells by downregulating basic leucine zipper ATF-like transcription factor (BATF) expression. Moreover, BATF promoted breast cancer cell migration and invasiveness by increasing TGFβ1 mRNA and protein levels. Bioinformatics analysis, dual luciferase reporter assays, and chromatin immunoprecipitation assays confirmed the presence of BATF-binding sites in the promoter sequence of TGFβ1 gene. Calycosin treatment inhibited epithelial-mesenchymal transition (EMT) of breast cancer cells by significantly increasing E-cadherin levels and decreasing N-cadherin, Vimentin, CD147, MMP-2, and MMP-9 levels through downregulation of BATF and TGFβ1. TGFβ1 knockdown reduced the migration and invasiveness of BATF-overexpressing breast cancer cells, whereas incubation with TGFβ1 enhanced the migration and invasiveness of Calycosin-treated breast cancer cells. Our findings demonstrated that Calycosin inhibited EMT and progression of breast cancer cells by suppressing BATF/TGFβ1 signaling. This suggests Calycosin would be a promising therapeutic option for breast cancer patients.

Calycosin ameliorates atherosclerosis by enhancing autophagy via regulating the interaction between KLF2 and MLKL in apolipoprotein E gene-deleted mice

Br J Pharmacol.2022 Jan;179(2):252-269. PMID: 34713437DOI: 10.1111/bph.15720

Background and purpose: Atherosclerosis is one of the underlying causes of cardiovascular disease. Formation of foam cells and necrotic core in the plaque is a hallmark of atherosclerosis, which results from lipid deposition, apoptosis, and inflammation in macrophages. Macrophage autophagy is a critical anti-atherogenic process and defective autophagy aggravates atherosclerosis by enhancing foam cell formation, apoptosis, and inflammation. Hence, enhancing autophagy can be a strategy for atherosclerosis treatment. Calycosin, a flavonoid from Radix Astragali, displays anti-oxidant and anti-inflammatory activities and therefore is potential to reduce the risk of cardiovascular disease. However, the anti-atherogenic effect of Calycosin and the involved mechanism remains unclear. In this study, we assessed the potential benefits of Calycosin on autophagy and atherosclerosis, and revealed the underlying mechanism. Experimental approach: In this study, apoE-/- mice were fed high-fat diet for 16 weeks in the presence of Calycosin and/or autophagy inhibitor chloroquine, which was followed by determination of atherosclerosis development, autophagy activity, and involved mechanisms. Key results: Calycosin protected against atherosclerosis and enhanced plaque stability via promoting autophagy. Calycosin inhibited foam cell formation, inflammation, and apoptosis by enhancing autophagy. MLKL was demonstrated as a new autophagy regulator, which can be negatively regulated by KLF2. Mechanistically, inhibitory effects of Calycosin on atherogenesis were via improved autophagy through KLF2-MLKL signalling pathway modulation. Conclusions and implications: This study demonstrated the atheroprotective effect of Calycosin was through upregulating KLF2-MLKL-mediated autophagy, which not only proposed novel mechanistic insights into t atherogenesis but also identified Calycosin as a potential drug candidate for atherosclerosis treatment.

Calycosin attenuates doxorubicin-induced cardiotoxicity via autophagy regulation in zebrafish models

Biomed Pharmacother.2021 May;137:111375.PMID: 33761601DOI:10.1016/j.biopha.2021.111375

cardiotoxicity is the main side effect with poor prognosis. No mechanism-based therapy is currently available to reverse chronic anthracycline-induced cardiotoxicity (AIC) after the deterioration of cardiac function. Calycosin (CA) is the main compound extracted from the traditional Chinese medicine Astragalus, and it has diverse beneficial effects, including autophagy modulation, anti-inflammatory and anti-tumor effects. Autophagy dysregulation is an important pathological event in AIC. Our study demonstrated a cardioprotective effect of CA in a zebrafish embryonic AIC model. To assess the effect of CA on late-onset chronic AIC, adult zebrafish were treated with CA 28 days after doxorubicin (DOX) injection, at which point heart function was obviously impaired. The results demonstrated that DOX blocked autophagic activity in adult zebrafish 8 weeks post-injection, and CA treatment improved heart function and restored autophagy. Further in vitro experiments demonstrated that atg7, which encodes an E1-like activating enzyme, may play an essential role in the CA regulation of autophagy. In conclusion, we used a rapid pharmacological screening system in embryo-adult zebrafish in vivo and elucidated the mechanism of gene targeting in vitro.