Chrysosplenol D
(Synonyms: 猫眼草酚D) 目录号 : GC64028
Chrysosplenol D 是一种甲氧基黄酮类化合物，可在三阴性人乳腺癌细胞中诱导 ERK1/2 介导的细胞凋亡。Chrysosplenol D 还具有抗炎和中等抗锥虫活性。
Cas No.:14965-20-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Chrysosplenol D is a methoxy flavonoid that induces ERK1/2-mediated apoptosis in triple negative human breast cancer cells. Chrysosplenol D also exhibits anti-inflammatory and moderate antitrypanosomal activities[1][2][3][4].
Chrysosplenol D inhibits the cell viability of CaCo2 cells, with IC50 of 63.48 μM[1].Chrysosplenol D (1-100 μM; 48 h) selectively inhibits the viability of the TNBC cell lines, MDA-MB-231, CAL-51, CAL-148, as well as MCF7, A549, MIA PaCa-2, and PC-3[2].Chrysosplenol D (1-10 μM; 48 h) induces cell cycle aberrations with accumulation of cells in the S-phase and partially in the G2/M-phase of the cell cycle[2].Chrysosplenol D (1-10 μM; 48 h) induce apoptosis in breast cancer cells[2].Chrysosplenol D shows moderate antitrypanosomal activity, with IC50 of 47.27 μM for T.b. brucei[3].
Chrysosplenol D (30 μM; 3 d) inhibits MDA-MB-231 tumor growth on chick chorioallantoic membranes[2].Chrysosplenol D (0.07-0.28 mmol/kg) protects against LPS-induced systemic inflammatory response syndrome (SIRS) in mice[4].Chrysosplenol D (1-1.5 μmol/cm2) inhibits croton oil-induced ear edema in mice[4].
[1]. Habib ES, et, al. Anti-inflammatory effect of methoxyflavonoids from Chiliadenus montanus (Jasonia Montana) growing in Egypt. Nat Prod Res. 2020 Aug 4;1-5.
[2]. Lang SJ, et, al. Chrysosplenol d, a Flavonol from Artemisia annua, Induces ERK1/2-Mediated Apoptosis in Triple Negative Human Breast Cancer Cells. Int J Mol Sci. 2020 Jun 8;21(11):4090.
[3]. Skaf J, et, al. Improving anti-trypanosomal activity of alkamides isolated from Achillea fragrantissima. Fitoterapia. 2018 Mar;125:191-198.
[4]. Li YJ, et, al. Flavonoids casticin and chrysosplenol D from Artemisia annua L. inhibit inflammation in vitro and in vivo. Toxicol Appl Pharmacol. 2015 Aug 1;286(3):151-8.
| Cas No. | 14965-20-9 | SDF | Download SDF |
| 别名 | 猫眼草酚D | ||
| 分子式 | C18H16O8 | 分子量 | 360.31 |
| 溶解度 | DMSO : 50 mg/mL (138.77 mM; Need ultrasonic) | 储存条件 | 4°C, away from moisture and light |
| 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 | 2.7754 mL | 13.8769 mL | 27.7539 mL |
| 5 mM | 0.5551 mL | 2.7754 mL | 5.5508 mL |
| 10 mM | 0.2775 mL | 1.3877 mL | 2.7754 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。
Chrysosplenol D Triggers Apoptosis through Heme Oxygenase-1 and Mitogen-Activated Protein Kinase Signaling in Oral Squamous Cell Carcinoma
Cancers (Basel) 2021 Aug 27;13(17):4327.PMID:34503136DOI:10.3390/cancers13174327.
Chrysosplenol D, a flavonol isolated from Artemisia annua L., can exert anticancer effects. This study investigated the anticancer property of Chrysosplenol D and its underlying mechanism in oral squamous cell carcinoma (OSCC). We observed that Chrysosplenol D reduced cell viability and caused cell cycle arrest in the G2/M phase. The findings of annexin V/propidium iodide staining, chromatin condensation, and apoptotic-related protein expression revealed that Chrysosplenol D regulated apoptosis in OSCC. Furthermore, Chrysosplenol D altered the expression of the autophagy marker LC3 and other autophagy-related proteins. Phosphatidylinositol 3-kinase/protein kinase B, extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase (MAPK) were downregulated by Chrysosplenol D, and the inhibition of these pathways significantly enhanced chrysosplenol D-induced cleaved poly (ADP-ribose) polymerase activation. Moreover, the upregulation of heme oxygenase-1 (HO-1) was found to be critical for chrysosplenol D-induced apoptotic cell death. The analysis of clinical data from The Cancer Genome Atlas and Gene Expression Omnibus datasets revealed that patients with head and neck cancer had lower HO-1 expression than did those with no head and neck cancer. The findings of the present study indicated that Chrysosplenol D exerts anticancer effects on OSCC by suppressing the MAPK pathway and activating HO-1 expression.
Chrysosplenol D, a Flavonol from Artemisia annua, Induces ERK1/2-Mediated Apoptosis in Triple Negative Human Breast Cancer Cells
Int J Mol Sci 2020 Jun 8;21(11):4090.PMID:32521698DOI:10.3390/ijms21114090.
Triple negative human breast cancer (TNBC) is an aggressive cancer subtype with poor prognosis. Besides the better-known artemisinin, Artemisia annua L. contains numerous active compounds not well-studied yet. High-performance liquid chromatography coupled with diode-array and mass spectrometric detection (HPLC-DAD-MS) was used for the analysis of the most abundant compounds of an Artemisia annua extract exhibiting toxicity to MDA-MB-231 TNBC cells. Artemisinin, 6,7-dimethoxycoumarin, arteannuic acid were not toxic to any of the cancer cell lines tested. The flavonols Chrysosplenol D and casticin selectively inhibited the viability of the TNBC cell lines, MDA-MB-231, CAL-51, CAL-148, as well as MCF7, A549, MIA PaCa-2, and PC-3. PC-3 prostate cancer cells exhibiting high basal protein kinase B (AKT) and no ERK1/2 activation were relatively resistant, whereas MDA-MB-231 cells with high basal ERK1/2 and low AKT activity were more sensitive to Chrysosplenol D treatment. In vivo, Chrysosplenol D and casticin inhibited MDA-MB-231 tumor growth on chick chorioallantoic membranes. Both compounds induced mitochondrial membrane potential loss and apoptosis. Chrysosplenol D activated ERK1/2, but not other kinases tested, increased cytosolic reactive oxygen species (ROS) and induced autophagy in MDA-MB-231 cells. Lysosomal aberrations and toxicity could be antagonized by ERK1/2 inhibition. The Artemisia annua flavonols Chrysosplenol D and casticin merit exploration as potential anticancer therapeutics.
Chrysosplenol D protects mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via TLR4-MAPKs/NF-κB signaling pathways
Innate Immun 2021 Oct;27(7-8):514-524.PMID:34806444DOI:10.1177/17534259211051069.
This study investigated the effect and mechanism of Chrysosplenol D (CD) on LPS-induced acute lung injury in mice. Histological changes in the lungs were measured by hematoxylin-eosin staining. The levels of IL-6, IL-1β, and TNF-α in the bronchoalveolar lavage fluid were detected by ELISA. The levels of oxidative stress were detected by the cuvette assay. Immune cells in peripheral blood, the levels of reactive oxygen species, and apoptosis of primary lung cells were detected by flow cytometry. The mRNA levels of TLR4, MyD88, IL-1β, and NLRP3 were measured by quantitative real-time polymerase chain reaction. The levels of proteins in apoptosis and the TLR4-MAPKs/NF-κB signaling pathways were detected by Western blot. Hematoxylin-eosin staining showed that CD could improve lung injury; decrease the levels of inflammatory factors, oxidative stress, reactive oxygen species, and cell apoptosis; and regulate the immune system. Moreover, CD could down-regulate the mRNA levels of TLR4, MyD88, NLRP3, and IL-1β in lung, and the protein levels of Keap-1, Cleaved-Caspase-3/Caspase-3, Cleaved-Caspase-9/Caspase-9, TLR4, MyD88, p-ERK/ERK, p-JNK/JNK, p-p38/p38, p-p65/p65, NLRP3, and IL-1β, and up-regulated the levels of Bcl-2/Bax, p-Nrf2/Nrf2, and HO-1. The results suggested that CD could protect mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via the TLR4-MAPKs/NF-κB signaling pathways.
Flavonoids casticin and Chrysosplenol D from Artemisia annua L. inhibit inflammation in vitro and in vivo
Toxicol Appl Pharmacol 2015 Aug 1;286(3):151-8.PMID:25891417DOI:10.1016/j.taap.2015.04.005.
Background: The aim of our experiments was to investigate the anti-inflammatory properties of casticin and Chrysosplenol D, two flavonoids present in Artemisia annua L. Methods: Topical inflammation was induced in ICR mice using croton oil. Mice were then treated with casticin or Chrysosplenol D. Cutaneous histological changes and edema were assessed. ICR mice were intragastrically administrated with casticin or Chrysosplenol D followed by intraperitoneal injection of lipopolysaccharide (LPS). Mouse Raw264.7 macrophage cells were incubated with casticin or Chrysosplenol D. Intracellular phosphorylation was detected, and migration was assessed by trans-well assay. HT-29/NFκB-luc cells were incubated with casticin or Chrysosplenol D in the presence or absence of LPS, and NF-κB activation was quantified. Results: In mice, administration of casticin (0.5, 1 and 1.5μmol/cm(2)) and Chrysosplenol D (1 and 1.5μmol/cm(2)) inhibited croton oil-induced ear edema (casticin: 29.39-64.95%; Chrysosplenol D: 37.76-65.89%, all P<0.05) in a manner similar to indomethacin (0.5, 1 and 1.5μmol/cm(2); 55.63-84.58%). Casticin (0.07, 0.13 and 0.27mmol/kg) and Chrysosplenol D (0.07, 0.14 and 0.28mmol/kg) protected against LPS-induced systemic inflammatory response syndrome (SIRS) in mice (all P<0.05), in a manner similar to dexamethasone (0.03mmol/kg). Casticin and Chrysosplenol D suppressed LPS-induced release of IL-1 beta, IL-6 and MCP-1, inhibited cell migration, and reduced LPS-induced IκB and c-JUN phosphorylation in Raw264.7 cells. JNK inhibitor SP600125 blocked the inhibitory effect of Chrysosplenol D on cytokine release. Conclusions: The flavonoids casticin and Chrysosplenol D from A. annua L. inhibited inflammation in vitro and in vivo.
Casticin and Chrysosplenol D from Artemisia annua L. induce apoptosis by inhibiting topoisomerase IIα in human non-small-cell lung cancer cells
Phytomedicine 2022 Jun;100:154095.PMID:35398735DOI:10.1016/j.phymed.2022.154095.
Background: Artemisia annua L. (A. annua) and its active components exhibit antitumour effects in many cancer cells. However, the biological processes and mechanisms involved are not well understood, especially for the treatment of non-small-cell lung cancer (NSCLC). Purpose: This study aimed to comprehensively explore the biological processes of A. annua and its active components in NSCLC cells and to identify the mechanism by which these compounds induce apoptosis. Study designs/methods: Cell viability and flow cytometry assays were used to evaluate the cytotoxicity of A. annua active components casticin (CAS) and Chrysosplenol D (CHD) in A. annua in NSCLC cells. After treatment with CAS and CHD, A549 cells were subjected to RNA sequencing (RNA-seq) analysis, differentially expressed genes (DEGs) were screened and subjected to functional enrichment analysis (KEGG and GO analysis) as well as protein interaction network analysis. The key targets associated with apoptosis induction in A549 cells were screened by Cytoscape, and the screened DEGs were validated by qRT-PCR. Immunoblotting, immunofluorescence, and molecular docking assays were used to determine whether CAS and/or CHD could induce apoptosis in NSCLC cells by inducing DNA damage through down-regulation of topoisomerase IIα (topo IIα) expression. The same experiments were verified again in the H1299 lung cancer cell line. Results: CAS and CHD inhibited NSCLC cells proliferation in a time- and dose-dependent manner, and significantly induced apoptosis. A total of 115 co-upregulated DEGs and 277 co-downregulated DEGs were identified in A549 cells following treatment with CAS and CHD. Comprehensive and systematic data about biological processes and mechanisms were obtained. DNA damage pathways and topo IIα targets were screened to study the apoptosis effects of CAS and CHD on NSCLC cells. CAS and CHD may be able to induce DNA damage by binding to topo IIα-DNA and reducing topo IIα activity. Conclusion: This study suggested that CAS and CHD may reduce topo IIα activity by binding to topo IIα-DNA, affecting the replication of DNA, triggering DNA damage, and inducing apoptosis. It described a novel mechanism associated with topo IIα inhibition to reveal a novel role for CAS and CHD in A. annua as potential anticancer agents and/or adjuvants in NSCLC cells.