Xanthoangelol
(Synonyms: 黄色当归醇) 目录号 : GC61382
Xanthoangelol, a chalcone found in the roots of Angelica keiskei, is a nonselective monoamine oxidase (MAO) inhibitor and a potent dopamine β-hydroxylase (DBH) inhibitor. It has anti-inflammatory, antibiotic and pro-apoptotic activities.
Cas No.:62949-76-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Xanthoangelol, a chalcone found in the roots of Angelica keiskei, is a nonselective monoamine oxidase (MAO) inhibitor and a potent dopamine β-hydroxylase (DBH) inhibitor. It has anti-inflammatory, antibiotic and pro-apoptotic activities.
[1] Kim JH, Biomol Ther (Seoul). 2013 May 30;21(3):234-40.
| Cas No. | 62949-76-2 | SDF | |
| 别名 | 黄色当归醇 | ||
| Canonical SMILES | O=C(/C=C/C1=CC=C(O)C=C1)C2=CC=C(O)C(C/C=C(C)/CC/C=C(C)/C)=C2O | ||
| 分子式 | C25H28O4 | 分子量 | 392.49 |
| 溶解度 | DMSO : 100 mg/mL (254.78 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.5478 mL | 12.7392 mL | 25.4784 mL |
| 5 mM | 0.5096 mL | 2.5478 mL | 5.0957 mL |
| 10 mM | 0.2548 mL | 1.2739 mL | 2.5478 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 | ||||||||||
| 计算重置 | ||||||||||
计算结果:
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Endoplasmic reticulum stress triggers Xanthoangelol-induced protective autophagy via activation of JNK/c-Jun Axis in hepatocellular carcinoma
J Exp Clin Cancer Res 2019 Jan 8;38(1):8.PMID:30621754DOI:10.1186/s13046-018-1012-z.
Background: Xanthoangelol (XAG) was reported to exhibit antitumor properties in several cancer. However, the specific anti-tumor activity of XAG in human hepatocellular carcinoma (HCC) and the relevant mechanisms are not known. Methods: The effects of XAG on HCC cell proliferation and apoptosis were respectively examined by CCK-8 assay and Annexin V-FITC/PI apoptosis kit. Western blotting was conducted to detect the expression of proteins. The effect of XAG on the development of acidic vesicle organelles was assessed using acridine orange staining. mRFP-GFP-LC3 adenovirus was used to transfect HCC cells and the formation of autolysosome was detected using a confocal microscope. Results: Mechanistically, XAG promotes HCC cell death through triggering intrinsic apoptosis pathway, not extrinsic apoptotic pathway. Furthermore, XAG treatment induced autophagy in Bel 7402 and SMMC 7721 cells, as evidenced by an increase in autophagy-associated proteins, including LC3B-II, Beclin-1, and Atg5. Interestingly, inhibition of autophagy with 3-MA, Bafilomycin A1 (Baf A1), or siRNA targeting Atg5 effectively enhanced the apoptotic cell ratio in XAG-treated cells, indicating that protective effect of autophagy induced by XAG in HCC. Moreover, autophagy induced by XAG was mediated by activating endoplasmic reticulum stress (ERS), along with administration of XAG, the expression levels of ERS-associated proteins, including CHOP, GRP78, ATF6, p-eIF2α, IRE1α, and cleaved caspase-12 were significantly increased in HCC cells. Meanwhile, suppressing ERS with chemical chaperones (TUDCA) or CHOP shRNA could effectively abrogate the autophagy-inducing effect of XAG, and increase the apoptotic cell death. Further mechanistic studies showed that ERS-induced autophagy in XAG-treated cells was mediated by activation of JNK/c-jun pathway. XAG treatment resulted in the increase of p-JNK and p-c-jun, while suppressing ERS with TUDCA or CHOP shRNA could effectively reverse it. Meanwhile, SP600125, a JNK inhibitor, effectively reversed XAG-induced protective autophagy and enhanced cell apoptosis in XAG-treated HCC cells. In vivo results demonstrated that XAG exerts potent antitumor properties with low toxicity. Conclusions: Collectively, these results suggested that XAG could be served as a promising candidate for the treatment and prevention of HCC.
Xanthoangelol alleviates cerebral ischemia reperfusion injury in rats
Anat Rec (Hoboken) 2021 Mar;304(3):602-612.PMID:32589370DOI:10.1002/ar.24481.
Ischemia/reperfusion (I/R) injury accounts to be a prime cause of neurological deficit following stroke. This study aimed to explore the neuro-protective effects of Xanthoangelol (XAG) on I/R-induced injury in both in vivo and in vitro models. Our data demonstrated that XAG can shrink infarct size and brain edema in middle cerebral artery occlusion (MCAO) model. In addition, XAG was capable of alleviating the neurological deficit in rats that have undergone MCAO procedure. Meanwhile, antiapoptotic activities of XAG against I/R-induced neuronal injury were evidenced and further illustrated that XAG elicits antiapoptotic activities by suppressing excessive oxidative stress via nuclear factor erythroid-2-related factor 2 activation. Overall, our study revealed that XAG displayed the potential to be utilized as a neuroprotective agent against I/R-induced neurological injury.
Pharmacological mechanism of Xanthoangelol underlying Nrf-2/TRPV1 and anti-apoptotic pathway against scopolamine-induced amnesia in mice
Biomed Pharmacother 2022 Jun;150:113073.PMID:35658216DOI:10.1016/j.biopha.2022.113073.
Alzheimer's disease (AD) is a well-known type of age-related dementia. The present study was conducted to investigate the effect of Xanthoangelol against memory deficit and neurodegeneration associated with AD. Preliminarily, Xanthoangelol produced neuroprotective effect against H2O2-induced HT-22 cells. Furthermore, effect of Xanthoangelol against scopolamine-induced amnesia in mice was determined by intraperitoneally (i.p.) administering Xanthoangelol (1, 10 and 20 mg/kg), 30 min prior to induction. Mice were administered scopolamine at a concentration of 1 mg/kg; i.p. for the induction of amnesia associated with AD. Xanthoangelol dose dependently reduced the symptoms of Alzheimer's disease as observed by the results obtained from the behavioral analysis performed using Morris water maze and Y-maze test. The immunohistochemical analysis suggested that Xanthoangelol significantly improved Keap-1/Nrf-2 signaling pathway. It greatly reduced the effects of oxidative stress and showed improvement in the anti-oxidant enzyme such as GSH, GST, SOD and catalase. Additionally, Xanthoangelol decreased the expression of transient receptor potential vanilloid 1 (TRPV-1), a nonselective cation channel, involved in synaptic plasticity and memory. It activated the anti-oxidants and attenuated the apoptotic (Bax/Bcl-2) pathway. Xanthoangelol also significantly attenuated the scopolamine-induced neuroinflammation by the inhibition of interleukin-1 beta (IL-1β), and tumor necrosis factor-α (TNF-α) levels. The histological analysis, showed a significant reduction in amyloid plaques by Xanthoangelol. Therefore, the present study indicated that Xanthoangelol has the ability to ameliorate the AD symptoms by attenuating neuroinflammation and neurodegeneration induced by scopolamine.
The plant-derived chalcone Xanthoangelol targets the membrane of Gram-positive bacteria
Bioorg Med Chem 2019 Dec 1;27(23):115151.PMID:31648878DOI:10.1016/j.bmc.2019.115151.
Xanthoangelol is a geranylated chalcone isolated from fruits of Amorpha fructicosa that exhibits antibacterial effects at low micromolar concentration against Gram-positive bacterial pathogens such as methicillin-resistant Staphylococcus aureus (MRSA), Enterococcus faecium and Enterococcus faecalis. We demonstrate that Xanthoangelol treatment of Gram-positive bacteria affects bacterial membrane integrity and leads to a leakage of intracellular metabolites. This correlates with a rapid collapse of the membrane potential and results in a fast and strong bactericidal effect. Proteomic profiling of Xanthoangelol-treated cells revealed signatures of cell wall and/or membrane damage and oxidative stress. Xanthoangelol specifically disturbs the membrane of Gram-positive bacteria potentially by forming pores resulting in cell lysis. In contrast, Xanthoangelol treatment of human cells showed only mildly hemolytic and cytotoxic effects at higher concentrations. Therefore, geranylated chalcones such as Xanthoangelol are promising lead structures for new antimicrobials against drug-resistant gram-positive pathogens.
Xanthoangelol and 4-hydroxyderrcin suppress obesity-induced inflammatory responses
Obesity (Silver Spring) 2016 Nov;24(11):2351-2360.PMID:27619735DOI:10.1002/oby.21611.
Objective: Obesity-induced inflammation plays a pivotal role in the pathogenesis of insulin resistance and type 2 diabetes. Xanthoangelol (XA) and 4-hydroxyderrcin (4-HD), phytochemicals extracted from Angelica keiskei, have been reported to possess various biological properties. Whether XA and 4-HD alleviate obesity-induced inflammation and inflammation-induced adipocyte dysfunction was investigated. Methods: For the in vitro study, a co-culture system composed of macrophages and adipocytes and macrophages stimulated with conditioned medium derived from fully differentiated adipocytes was conducted. For the in vivo study, mice were fed a high-fat diet supplemented with XA for 14 weeks. Results: XA and 4-HD suppressed inflammatory factors in co-culture system. Moreover, treatment of RAW macrophages with XA and 4-HD moderated the suppression of uncoupling protein 1 promoter activity and gene expression in C3H10T1/2 adipocytes, which was induced by conditioned medium derived from LPS-stimulated RAW macrophages. Also, XA and 4-HD inhibited c-Jun N-terminal kinase phosphorylation, nuclear factor-κB, and activator protein 1, the last two being transcription activators in activated macrophages. Furthermore, in mice fed the high-fat diet, XA reduced inflammatory factors within the white adipose tissue. Conclusions: These results suggest that XA and 4-HD might be promising phytochemicals to suppress obesity-induced inflammation and inflammation-induced adipocyte dysfunction.