| InChI=1S/C14H8O4/c15-9-5-1-3-7-11(9)14(18)12-8(13(7)17)4-2-6-10(12)16/h1-6,15-16H |
| QBPFLULOKWLNNW-UHFFFAOYSA-N |
| Oc1cccc2C(=O)c3cccc(O)c3C(=O)c12 |
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apoptosis inducer
Any substance that induces the process of apoptosis (programmed cell death) in multi-celled organisms.
plant metabolite
Any eukaryotic metabolite produced during a metabolic reaction in plants, the kingdom that include flowering plants, conifers and other gymnosperms.
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View more via ChEBI Ontology
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1,8-dihydroxyanthracene-9,10-dione
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dantron
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ChEBI
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dantrona
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ChemIDplus
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dantrone
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ChemIDplus
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dantronum
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ChemIDplus
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1,8-dihydroxy-9,10-anthracenedione
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NIST Chemistry WebBook
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1,8-dihydroxy-9,10-anthraquinone
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IUPAC
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1,8-dihydroxyanthra-9,10-quinone
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NIST Chemistry WebBook
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1,8-Dihydroxyanthrachinon
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NIST Chemistry WebBook
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1,8-Dihydroxyanthraquinone
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KEGG COMPOUND
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Chrysazin
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KEGG COMPOUND
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Chrysazin
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KEGG COMPOUND
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Danthron
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KEGG COMPOUND
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Dioxyanthrachinonum
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ChemIDplus
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3125
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DrugCentral
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C00002804
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KNApSAcK
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C10312
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KEGG COMPOUND
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CHZ
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PDBeChem
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D07107
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KEGG DRUG
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DB04816
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DrugBank
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HMDB0029752
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HMDB
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LSM-2208
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LINCS
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| View more database links |
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117-10-2
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CAS Registry Number
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KEGG COMPOUND
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117-10-2
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CAS Registry Number
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ChemIDplus
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117-10-2
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CAS Registry Number
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NIST Chemistry WebBook
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2054727
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Reaxys Registry Number
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Reaxys
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29905
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Gmelin Registry Number
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Gmelin
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Verebová V, Adamcik J, Danko P, Podhradský D, Miškovský P, Staničová J (2014)
Anthraquinones quinizarin and danthron unwind negatively supercoiled DNA and lengthen linear DNA.
Biochemical and biophysical research communications 444, 50-55 [PubMed:24434150]
[show Abstract]
The intercalating drugs possess a planar aromatic chromophore unit by which they insert between DNA bases causing the distortion of classical B-DNA form. The planar tricyclic structure of anthraquinones belongs to the group of chromophore units and enables anthraquinones to bind to DNA by intercalating mode. The interactions of simple derivatives of anthraquinone, quinizarin (1,4-dihydroxyanthraquinone) and danthron (1,8-dihydroxyanthraquinone), with negatively supercoiled and linear DNA were investigated using a combination of the electrophoretic methods, fluorescence spectrophotometry and single molecule technique an atomic force microscopy. The detection of the topological change of negatively supercoiled plasmid DNA, unwinding of negatively supercoiled DNA, corresponding to appearance of DNA topoisomers with the low superhelicity and an increase of the contour length of linear DNA in the presence of quinizarin and danthron indicate the binding of both anthraquinones to DNA by intercalating mode. | Zhou R, Wang L, Xu X, Chen J, Hu LH, Chen LL, Shen X (2013)
Danthron activates AMP-activated protein kinase and regulates lipid and glucose metabolism in vitro.
Acta pharmacologica Sinica 34, 1061-1069 [PubMed:23770982]
[show Abstract]
AimTo discover the active compound on AMP-activated protein kinase (AMPK) activation and investigate the effects of the active compound 1,8-dihydroxyanthraquinone (danthron) from the traditional Chinese medicine rhubarb on AMPK-mediated lipid and glucose metabolism in vitro.MethodsHepG2 and C2C12 cells were used. Cell viability was determined using MTT assay. Real-time PCR was performed to measure the gene expression. Western blotting assay was applied to investigate the protein phosphorylation level. Enzymatic assay kits were used to detect the total cholesterol (TC), triglyceride (TG) and glucose contents.ResultsDanthron (0.1, 1, and 10 μmol/L) dose-dependently promoted the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) in both HepG2 and C2C12 cells. Meanwhile, danthron treatment significantly reduced the lipid synthesis related sterol regulatory element-binding protein 1c (SREBP1c) and fatty acid synthetase (FAS) gene expressions, and the TC and TG levels. In addition, danthron treatment efficiently increased glucose consumption. The actions of danthron on lipid and glucose metabolism were abolished or reversed by co-treatment with the AMPK inhibitor compound C.ConclusionDanthron effectively reduces intracellular lipid contents and enhanced glucose consumption in vitro via activation of AMPK signaling pathway. | Chiou SM, Chiu CH, Yang ST, Yang JS, Huang HY, Kuo CL, Chen PY, Chung JG (2012)
Danthron triggers ROS and mitochondria-mediated apoptotic death in C6 rat glioma cells through caspase cascades, apoptosis-inducing factor and endonuclease G multiple signaling.
Neurochemical research 37, 1790-1800 [PubMed:22592642]
[show Abstract]
This research focused on the induction of cytotoxic effects by danthron, a natural anthraquinone derivative on C6 rat glioma cells through exploring the means of cell death and the effects on mitochondrial function. We found that danthron decreased the percentage of viable C6 cells and induced cell morphological changes in a dose-and time-dependent manner. The morphological and nuclei changes (DAPI staining) in C6 cells were observed using a contrast-microscope and fluorescence microscopy, respectively. The results suggest that cell death of C6 cells which are induced by danthron is closely related to apoptotic death. Danthron decreased the level of mitochondrial membrane potential (ΔΨ( m )), stimulated the release of cytochrome c from mitochondria to cytosol and promoted the levels of caspase-9 and caspase-3, or induced the release of AIF and Endo G from mitochondria. Based on both observations, we suggest that the danthron-provoked apoptotic death of C6 cells is mediated through the mitochondria-dependent pathway. Furthermore, our results also indicated that danthron triggered apoptosis through reactive oxygen species (ROS) production which were increased after 1 h exposure of danthron, which was reversed by the ROS scavenger N-acetyl-L: -cysteine (NAC). As a consequence, danthron-mediated cell death of C6 cells via ROS production, mitochondrial transmembrane potential collapse and releases of cytochrome c, AIF and Endo G. Taken together, danthron was demonstrated to be effective in killing C6 rat glioma cells via the ROS-promoted and mitochondria-dependent apoptotic pathways. | Chen YL, Lu HF, Hung FM, Huang AC, Hsueh SC, Liu CM, Yang JS, Yu CC, Chiang JH, Lu CC, Chiu TH, Chung JG (2011)
Danthron inhibits murine WEHI-3 cells in vivo, and enhances macrophage phagocytosis and natural killer cell cytotoxic activity in leukemic mice.
In vivo (Athens, Greece) 25, 393-398 [PubMed:21576413]
[show Abstract]
Danthron has been shown to induce apoptotic cell death, and inhibit migration and invasion of human gastric or brain cancer cells in vitro. However, there is no report addressing whether danthron affects murine leukemia cells or immune responses in vivo. Herein, this study focused on the in-vivo effects of danthron on WEHI-3 leukemia in mice and immune responses in vivo. The results indicated that danthron reduced spleen weight and increased the percentage of cells with CD3 and CD19 markers, indicating that differentiation of the precursors of T- and B-cells was promoted in the leukemic mice. The results also showed that danthron promoted the activity of phagocytosis by macrophages isolated from the peritoneal cavity but had no effect on peripheral blood mononuclear cells. Danthron also promoted natural killer cell cytocytic activity at an effector and target cell ratio of 100:1 in comparison with leukemic animals in vivo. Taken together, these results demonstrated that application of danthron might affect WEHI-3 leukemia in mice and modulate immune responses in vivo. | Lu HF, Wang HL, Chuang YY, Tang YJ, Yang JS, Ma YS, Chiang JH, Lu CC, Yang JL, Lai TY, Wu CC, Chung JG (2010)
Danthron induced apoptosis through mitochondria- and caspase-3-dependent pathways in human brain glioblastoma multiforms GBM 8401 cells.
Neurochemical research 35, 390-398 [PubMed:19784869]
[show Abstract]
Danthron (1,8-dihydroxyanthraquinone), is one of component from Rheum palmatum L. (Polygonaceae), has been shown several biological activities but did not show to induce apoptosis in human brain tumor cells. The aim of this study is to investigate the mechanisms by danthron for the induction of apoptotic potential on human brain glioblastoma multiforms GBM 8401 cell line. Danthron showed a marked concentration- and time-dependent inhibition of GBM 8401 cell viability and induced apoptosis in a dose-and time-dependent manner. There was an attenuation of mitochondrial membrane potential (DeltaPsi(m)) with the alterations of Bcl-2/Bax protein ratio in GBM 8401 cells, indicating the participation of a mitochondria-related mechanism. Pretreatment of a caspase-8 inhibitor (Z-IETD-FMK), caspase-9 inhibitor (Z-LEHD-FMK) and caspase-3 inhibitor (Z-DEVE-FMK) significantly increased the viable of GBM 8401 cells implied that the participations of caspases. Western blotting analysis also showed the activation of initiator caspase-8 and caspase-9, and executor caspase-3 in GBM 8401 cells. Meanwhile, danthron also promoted the generation of reactive oxygen species (ROS) and cytosolic Ca(2+) in GBM 8401 cells. Taken together, our data showed that danthron induced apoptosis in GBM 8401 cells through mitochondria-related and caspase-related pathways, and it may be further evaluated as a chemotherapeutic agent for human brain cancer. | Lu HF, Lai TY, Hsia TC, Tang YJ, Yang JS, Chiang JH, Lu CC, Liu CM, Wang HL, Chung JG (2010)
Danthron induces DNA damage and inhibits DNA repair gene expressions in GBM 8401 human brain glioblastoma multiforms cells.
Neurochemical research 35, 1105-1110 [PubMed:20369292]
[show Abstract]
Our primary studies had shown that danthron induced cytotoxic effects, including apoptosis and inhibition of migration and invasion. However, danthron-affected DNA damage and repair gene expressions are not clear. In this study, we investigated to examine whether or not danthron induced DNA damage and inhibited DNA repair gene expression in human brain glioblastoma multiforms (GBM 8401) cells. The results from Comet assay indicated that incubation of GBM 8401 cells with 0, 50, 100 and 150 microM of danthron led to a longer DNA migration smear based on the single cell electrophoresis (Comet tail). The results from real-time PCR assay demonstrated that 100 microM of danthron for 24 h treatment in GBM 8401 cells led to decrease all examined ataxia telangiectasia mutated (ATM), ataxia-telangiectasia and Rad3-related (ATR), breast cancer 1, early onset (BRCA-1), 14-3-3 proteins sigma (14-3-3sigma), DNA-dependent serine/threonine protein kinase (DNA-PK) and O ( 6 )-methylguanine-DNA methyltransferase (MGMT) mRNA expressions. Taken together, the present study showed that danthron caused DNA damage and inhibited DNA repair genes, which may be the factors for danthron-inhibited cell growth in vitro. |
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