Chrysophanol

CAS# 481-74-3

Chrysophanol

Catalog No. BCN5567----Order now to get a substantial discount!

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Quality Control of Chrysophanol

Number of papers citing our products

Chemical structure

Chrysophanol

3D structure

Chemical Properties of Chrysophanol

Cas No. 481-74-3 SDF Download SDF
PubChem ID 10208 Appearance Yellow-orange powder
Formula C15H10O4 M.Wt 254.2
Type of Compound Anthraquinones Storage Desiccate at -20°C
Synonyms Chrysophanic acid
Solubility DMSO : 2 mg/mL (7.87 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
Chemical Name 1,8-dihydroxy-3-methylanthracene-9,10-dione
SMILES CC1=CC(=C2C(=C1)C(=O)C3=C(C2=O)C(=CC=C3)O)O
Standard InChIKey LQGUBLBATBMXHT-UHFFFAOYSA-N
Standard InChI InChI=1S/C15H10O4/c1-7-5-9-13(11(17)6-7)15(19)12-8(14(9)18)3-2-4-10(12)16/h2-6,16-17H,1H3
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Chrysophanol

1 Asphodelus sp. 2 Cassia sp. 3 Fallopia sp. 4 Harungana sp. 5 Polygonum sp. 6 Rhamnus sp. 7 Rheum sp.

Biological Activity of Chrysophanol

DescriptionChrysophanol (Chrysophanic acid) is a natural anthraquinone, which inhibits EGF-induced phosphorylation of EGFR and suppresses activation of AKT and mTOR/p70S6K. Chrysophanol has anti-inflammatory, cytotoxicity and anti-diabetic properties, it can play metabolic roles in the insulin-stimulated glucose transport pathway; it can inhibit NALP3 inflammasome activation and ameliorate cerebral ischemia/reperfusion in mice; it also is active against plant powdery mildew.
TargetsROS | NF-kB | Caspase | Calcium Channel | GLUT | TNF-α | COX | IL Receptor | EGFR | mTOR
In vitro

Chrysophanol-induced cell death (necrosis) in human lung cancer A549 cells is mediated through increasing reactive oxygen species and decreasing the level of mitochondrial membrane potential.[Pubmed: 22848001]

Environ Toxicol. 2014 May;29(7):740-9.

Chrysophanol (1,8-dihydroxy-3-methylanthraquinone) is one of the anthraquinone compounds, and it has been shown to induce cell death in different types of cancer cells. The effects of Chrysophanol on human lung cancer cell death have not been well studied.
METHODS AND RESULTS:
The purpose of this study is to examine Chrysophanol-induced cytotoxic effects and also to investigate such influences that involved apoptosis or necrosis in A549 human lung cancer cells in vitro. Our results indicated that Chrysophanol decreased the viable A549 cells in a dose- and time-dependent manner. Chrysophanol also promoted the release of reactive oxygen species (ROS) and Ca(2+) and decreased the levels of mitochondria membrane potential (ΔΨm ) and adenosine triphosphate in A549 cells. Furthermore, Chrysophanol triggered DNA damage by using Comet assay and DAPI staining. Importantly, Chrysophanol only stimulated the cytocheome c release, but it did not activate other apoptosis-associated protein levels including caspase-3, caspase-8, Apaf-1, and AIF.
CONCLUSIONS:
In conclusion, human lung cancer A549 cells treated with Chrysophanol exhibited a cellular pattern associated with necrotic cell death and not apoptosis in vitro.

Synergistic interaction of physcion and chrysophanol on plant powdery mildew.[Pubmed: 17397111]

Pest Manag Sci. 2007 May;63(5):511-5.

The extract of the plant Rheum officinale Baill, mainly containing the anthraquinones physcion and Chrysophanol, is highly active against plant powdery mildew.
METHODS AND RESULTS:
Experiments were conducted in the laboratory and greenhouse to determine the interaction of the two compounds on cucumber powdery mildew [Sphaerotheca fuliginea (Schlecht.) Poll] and on wheat powdery mildew [Blumeria graminis (DC.) Speer f. sp. tritici Marchal]. Physcion was much more bioactive than Chrysophanol against these powdery mildews. There was a significant synergistic interaction between the two compounds on the diseases when the ratios of physcion to Chrysophanol ranged from 1:9 to 5:5. The synergistic degree increased with increase in the Chrysophanol proportion in the combination.
CONCLUSIONS:
The findings indicate that, in order to ensure constant efficacy of the extract on the disease, both the contents and the proportion of the main active ingredients physcion and Chrysophanol have to be determined.

Anti-diabetic properties of chrysophanol and its glucoside from rhubarb rhizome.[Pubmed: 18981591]

Biol Pharm Bull. 2008 Nov;31(11):2154-7.

An ethanol extract of rhubarb rhizome exhibited marked glucose transport activity in differentiated L6 rat myotubes. Activity-guided fractionation resulted in the isolation of two anthraquinones, Chrysophanol-8-O-beta-D-glucopyranoside (1) and Chrysophanol (2).
METHODS AND RESULTS:
The anti-diabetic effect was examined by glucose transport activity, glucose transporter 4 (Glut4) expression in myotubes, and the level of insulin receptor (IR) tyrosine phosphorylation as influenced by tyrosine phosphatase 1B, each of which is a major target of diabetes treatment. Chrysophanol-8-O-beta-D-glucopyranoside up to 25 microM dose-dependently activated glucose transport in insulin-stimulated myotubes. Increased tyrosine phosphorylation of IR due to tyrosine phosphatase 1B inhibitory activity with an IC50 value of 18.34+/-0.29 microM and unchanged Glut4 mRNA levels was observed following Chrysophanol-8-O-beta-D-glucopyranoside treatment. Chrysophanol up to 100 microM exerted mild glucose transport activity and elevated the tyrosine phosphorylation of IR via tyrosine phosphatase 1B inhibition (IC50=79.86+/-0.12 microM); Glut4 mRNA expression was also significantly increased by 100 microM. The ED50 values of the two compounds were 59.38+/-0.66 and 79.69+/-0.03 microM, respectively.
CONCLUSIONS:
Therefore, these two anthraquinones from rhubarb rhizome, Chrysophanol-8-O-beta-D-glucopyranoside and Chrysophanol, have mild cytotoxicity and anti-diabetic properties and could play metabolic roles in the insulin-stimulated glucose transport pathway.

In vivo

Chrysophanol attenuates lead exposure-induced injury to hippocampal neurons in neonatal mice.[Pubmed: 25206913]

Neural Regen Res. 2014 May 1;9(9):924-30.

Previous studies have shown that Chrysophanol protects against learning and memory impairments in lead-exposed adult mice.
METHODS AND RESULTS:
In the present study, we investigated whether Chrysophanol can alleviate learning and memory dysfunction and hippocampal neuronal injury in lead-exposed neonatal mice. At the end of lactation, Chrysophanol (0.1, 1.0, 10.0 mg/kg) was administered to the neonatal mice by intraperitoneal injection for 15 days. Chrysophanol significantly alleviated injury to hippocampal neurons and improved learning and memory abilities in the lead-poisoned neonatal mice. Chrysophanol also significantly decreased lead content in blood, brain, heart, spleen, liver and kidney in the lead-exposed neonatal mice. The levels of malondialdehyde in the brain, liver and kidney were significantly reduced, and superoxide dismutase and glutathione peroxidase activities were significantly increased after Chrysophanol treatment.
CONCLUSIONS:
Collectively, these findings indicate that Chrysophanol can significantly reduce damage to hippocampal neurons in lead-exposed neonatal mice.

Protocol of Chrysophanol

Cell Research

Anti-Inflammatory activity of chrysophanol through the suppression of NF-kappaB/caspase-1 activation in vitro and in vivo.[Pubmed: 20877234 ]

Chrysophanol induces necrosis through the production of ROS and alteration of ATP levels in J5 human liver cancer cells.[Pubmed: 20169580 ]

Mol Nutr Food Res. 2010 Jul;54(7):967-76.

Anthraquinone compounds have been shown to induce apoptosis in different cancer cell types. Effects of Chrysophanol, an anthraquinone compound, on cancer cell death have not been well studied.
METHODS AND RESULTS:
The goal of this study was to examine if Chrysophanol had cytotoxic effects and if such effects involved apoptosis or necrosis in J5 human liver cancer cells. Chrysophanol induced necrosis in J5 cells in a dose- and time-dependent manner. Non-apoptotic cell death was induced by Chrysophanol in J5 cells and was characterized by caspase independence, delayed externalization of phosphatidylserine and plasma membrane disruption. Blockage of apoptotic induction by a general caspase inhibitor (z-VAD-fmk) failed to protect cells against Chrysophanol-induced cell death. The levels of reactive oxygen species production and loss of mitochondrial membrane potential (DeltaPsi(m)) were also determined to assess the effects of Chrysophanol. However, reductions in adenosine triphosphate levels and increases in lactate dehydrogenase activity indicated that Chrysophanol stimulated necrotic cell death.
CONCLUSIONS:
In summary, human liver cancer cells treated with Chrysophanol exhibited a cellular pattern associated with necrosis and not apoptosis.

Molecules. 2010 Sep 16;15(9):6436-51.

Chrysophanol is a member of the anthraquinone family and has multiple pharmacological effects, but the exact mechanism of the anti-inflammatory effects of Chrysophanol has yet to be thoroughly elucidated. In this study, we attempted to determine the effects of Chrysophanol on dextran sulfate sodium (DSS)-induced colitis and lipopolysaccharide (LPS)-induced inflammatory responses in mouse peritoneal macrophages. The findings of this study demonstrated that Chrysophanol effectively attenuated overall clinical scores as well as various pathological markers of colitis. Additionally, Chrysophanol inhibited the production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and the expression of cyclooxygenase (COX)-2 levels induced by LPS. We showed that this anti-inflammatory effect of Chrysophanol is through suppression of the activation of NF-kappaB and caspase-1 in LPS-stimulated macrophages. These results provide novel insights into the pharmacological actions of Chrysophanol as a potential molecule for use in the treatment of inflammatory diseases.

Animal Research

Chrysophanol inhibits NALP3 inflammasome activation and ameliorates cerebral ischemia/reperfusion in mice.[Pubmed: 24876671]

Mediators Inflamm. 2014;2014:370530.

The most effective way to contain cerebral ischemic injury is reperfusion; however, reperfusion itself may result in tissue injury, for which inflammatory damage is one of the main causative factors. NALP3 inflammasome is a multiprotein complex. It consists of NALP3, ASC, and caspase-1, whose function is to switch on the inflammatory process. Chrysophanol is an extract from plants of Rheum genus and it possesses many pharmacological effects including its anti-inflammation activity.
METHODS AND RESULTS:
In this study, the effects of Chrysophanol in cerebral ischemia/reperfusion and the potential mechanisms were investigated. Male CD1 mice were subject to transient middle cerebral artery occlusion (tMCAO). The NALP3 inflammasome activation status and its dynamic expression during the natural inflammatory response induced by tMCAO were first profiled. The neuroprotective effects of Chrysophanol were then assessed and the potential mechanisms mediating the observed neuroprotection were then explored. Physical parameters including neurological deficit, infarct size, brain edema, and BBB permeability were measured at 24 h after tMCAO. Confocal microscopy, Western blotting, immunohistochemistry, and qRT-PCR techniques were utilized to analyze the expression of NALP3 inflammasome and IL-1 β .
CONCLUSIONS:
Our results indicated that the brain tissue damage during cerebral ischemia/reperfusion is accompanied by NALP3 inflammasome activation. Chrysophanol could inhibit the activation of NALP3 inflammasome and protect cerebral ischemic stroke.

Chrysophanol Dilution Calculator

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Chrysophanol Molarity Calculator

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Preparing Stock Solutions of Chrysophanol

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.9339 mL 19.6696 mL 39.3391 mL 78.6782 mL 98.3478 mL
5 mM 0.7868 mL 3.9339 mL 7.8678 mL 15.7356 mL 19.6696 mL
10 mM 0.3934 mL 1.967 mL 3.9339 mL 7.8678 mL 9.8348 mL
50 mM 0.0787 mL 0.3934 mL 0.7868 mL 1.5736 mL 1.967 mL
100 mM 0.0393 mL 0.1967 mL 0.3934 mL 0.7868 mL 0.9835 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Chrysophanol

Chrysophanol (Chrysophanic acid) is a natural anthraquinone, which inhibits EGF-induced phosphorylation of EGFR and suppresses activation of AKT and mTOR/p70S6K.

In Vitro:Chrysophanol (Chrysophanic Acid) blocks proliferation of colon cancer cells by inhibiting EGFR/mTOR pathway. Chrysophanol, a natural anthraquinone, has anticancer activity in EGFR-overexpressing SNU-C5 human colon cancer cells. Chrysophanol treatment in SNU-C5 cells inhibits EGF-induced phosphorylation of EGFR and suppresses activation of downstream signaling molecules, such as AKT, extracellular signal-regulated kinase (ERK) and the mammalian target of Rapamycin (mTOR)/ribosomal protein S6 kinase (p70S6K). Chrysophanol (80 and 120 μM) significantly blocks cell proliferation when combined with the mTOR inhibitor, Rapamycin. Chrysophanol inhibits EGF-induced phosphorylation of EGFR and suppresses activation of AKT and mTOR/p70S6K, and significantly blocks cell proliferation. Chrysophanol dose dependently decreases CCK-8 and the viability of EGFR-overexpressing SNU-C5 cells. Chrysophanol treatment dose-dependently decreases EGF induced phosphorylation of EGFR at Tyr1068. Chrysophanol (80 and 120 μM) reduces the phosphorylation levels of mTOR at Ser2448. Chrysophanol (80 and 120 μM) also decreases the phosphorylation levels of p70S6K at Thr389. Chrysophanol inhibits EGF-induced EGFR activation and suppresses activation of the downstream signaling molecules, AKT and mTOR/p70S6K[1]. Chrysophanol (CA) inhibits lipid accumulation in 3T3-L1 adipocytes. Chrysophanol down-regulates adipogenic factors in 3T3-L1 adipocytes. Chrysophanol induces thermogenic factors in primary cultured brown adipocytes. Chrysophanol suppresses adipogenesis and induces thermogenesis via activation of AMPK pathway[2].

In Vivo:Chrysophanol (CA) improves HFD-induced obesity in C57BL/6 Mice. The in vivo performance of Chrysophanol is performed in male C57BL/6J mice to determine the efficacy of administered Chrysophanol. Mice fed the HFD gained significantly more weight than those fed the standard diet mice. On the other hand, weight gain of Chrysophanol group is significantly less than with the untreated HFD. Mice in the HFD-group gained 23.92 ± 1.74 g of weight, while those in the Chrysophanol group gained 16.72±2 g of weight after 16 weeks[2].

References:
[1]. Lee MS, et al. Chrysophanic acid blocks proliferation of colon cancer cells by inhibiting EGFR/mTOR pathway. Phytother Res. 2011 Jun;25(6):833-7. [2]. Lim H, et al. Chrysophanic Acid Suppresses Adipogenesis and Induces Thermogenesis by Activating AMP-Activated Protein Kinase Alpha In vivo and In vitro. Front Pharmacol. 2016 Dec 8;7:476.

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References on Chrysophanol

Anti-diabetic properties of chrysophanol and its glucoside from rhubarb rhizome.[Pubmed:18981591]

Biol Pharm Bull. 2008 Nov;31(11):2154-7.

An ethanol extract of rhubarb rhizome exhibited marked glucose transport activity in differentiated L6 rat myotubes. Activity-guided fractionation resulted in the isolation of two anthraquinones, Chrysophanol-8-O-beta-D-glucopyranoside (1) and Chrysophanol (2). The anti-diabetic effect was examined by glucose transport activity, glucose transporter 4 (Glut4) expression in myotubes, and the level of insulin receptor (IR) tyrosine phosphorylation as influenced by tyrosine phosphatase 1B, each of which is a major target of diabetes treatment. Chrysophanol-8-O-beta-D-glucopyranoside up to 25 microM dose-dependently activated glucose transport in insulin-stimulated myotubes. Increased tyrosine phosphorylation of IR due to tyrosine phosphatase 1B inhibitory activity with an IC50 value of 18.34+/-0.29 microM and unchanged Glut4 mRNA levels was observed following Chrysophanol-8-O-beta-D-glucopyranoside treatment. Chrysophanol up to 100 microM exerted mild glucose transport activity and elevated the tyrosine phosphorylation of IR via tyrosine phosphatase 1B inhibition (IC50=79.86+/-0.12 microM); Glut4 mRNA expression was also significantly increased by 100 microM. The ED50 values of the two compounds were 59.38+/-0.66 and 79.69+/-0.03 microM, respectively. Therefore, these two anthraquinones from rhubarb rhizome, Chrysophanol-8-O-beta-D-glucopyranoside and Chrysophanol, have mild cytotoxicity and anti-diabetic properties and could play metabolic roles in the insulin-stimulated glucose transport pathway.

Chrysophanol inhibits NALP3 inflammasome activation and ameliorates cerebral ischemia/reperfusion in mice.[Pubmed:24876671]

Mediators Inflamm. 2014;2014:370530.

The most effective way to contain cerebral ischemic injury is reperfusion; however, reperfusion itself may result in tissue injury, for which inflammatory damage is one of the main causative factors. NALP3 inflammasome is a multiprotein complex. It consists of NALP3, ASC, and caspase-1, whose function is to switch on the inflammatory process. Chrysophanol is an extract from plants of Rheum genus and it possesses many pharmacological effects including its anti-inflammation activity. In this study, the effects of Chrysophanol in cerebral ischemia/reperfusion and the potential mechanisms were investigated. Male CD1 mice were subject to transient middle cerebral artery occlusion (tMCAO). The NALP3 inflammasome activation status and its dynamic expression during the natural inflammatory response induced by tMCAO were first profiled. The neuroprotective effects of Chrysophanol were then assessed and the potential mechanisms mediating the observed neuroprotection were then explored. Physical parameters including neurological deficit, infarct size, brain edema, and BBB permeability were measured at 24 h after tMCAO. Confocal microscopy, Western blotting, immunohistochemistry, and qRT-PCR techniques were utilized to analyze the expression of NALP3 inflammasome and IL-1 beta . Our results indicated that the brain tissue damage during cerebral ischemia/reperfusion is accompanied by NALP3 inflammasome activation. Chrysophanol could inhibit the activation of NALP3 inflammasome and protect cerebral ischemic stroke.

Chrysophanol attenuates lead exposure-induced injury to hippocampal neurons in neonatal mice.[Pubmed:25206913]

Neural Regen Res. 2014 May 1;9(9):924-30.

Previous studies have shown that Chrysophanol protects against learning and memory impairments in lead-exposed adult mice. In the present study, we investigated whether Chrysophanol can alleviate learning and memory dysfunction and hippocampal neuronal injury in lead-exposed neonatal mice. At the end of lactation, Chrysophanol (0.1, 1.0, 10.0 mg/kg) was administered to the neonatal mice by intraperitoneal injection for 15 days. Chrysophanol significantly alleviated injury to hippocampal neurons and improved learning and memory abilities in the lead-poisoned neonatal mice. Chrysophanol also significantly decreased lead content in blood, brain, heart, spleen, liver and kidney in the lead-exposed neonatal mice. The levels of malondialdehyde in the brain, liver and kidney were significantly reduced, and superoxide dismutase and glutathione peroxidase activities were significantly increased after Chrysophanol treatment. Collectively, these findings indicate that Chrysophanol can significantly reduce damage to hippocampal neurons in lead-exposed neonatal mice.

Anti-Inflammatory activity of chrysophanol through the suppression of NF-kappaB/caspase-1 activation in vitro and in vivo.[Pubmed:20877234]

Molecules. 2010 Sep 16;15(9):6436-51.

Chrysophanol is a member of the anthraquinone family and has multiple pharmacological effects, but the exact mechanism of the anti-inflammatory effects of Chrysophanol has yet to be thoroughly elucidated. In this study, we attempted to determine the effects of Chrysophanol on dextran sulfate sodium (DSS)-induced colitis and lipopolysaccharide (LPS)-induced inflammatory responses in mouse peritoneal macrophages. The findings of this study demonstrated that Chrysophanol effectively attenuated overall clinical scores as well as various pathological markers of colitis. Additionally, Chrysophanol inhibited the production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and the expression of cyclooxygenase (COX)-2 levels induced by LPS. We showed that this anti-inflammatory effect of Chrysophanol is through suppression of the activation of NF-kappaB and caspase-1 in LPS-stimulated macrophages. These results provide novel insights into the pharmacological actions of Chrysophanol as a potential molecule for use in the treatment of inflammatory diseases.

Chrysophanol induces necrosis through the production of ROS and alteration of ATP levels in J5 human liver cancer cells.[Pubmed:20169580]

Mol Nutr Food Res. 2010 Jul;54(7):967-76.

Anthraquinone compounds have been shown to induce apoptosis in different cancer cell types. Effects of Chrysophanol, an anthraquinone compound, on cancer cell death have not been well studied. The goal of this study was to examine if Chrysophanol had cytotoxic effects and if such effects involved apoptosis or necrosis in J5 human liver cancer cells. Chrysophanol induced necrosis in J5 cells in a dose- and time-dependent manner. Non-apoptotic cell death was induced by Chrysophanol in J5 cells and was characterized by caspase independence, delayed externalization of phosphatidylserine and plasma membrane disruption. Blockage of apoptotic induction by a general caspase inhibitor (z-VAD-fmk) failed to protect cells against Chrysophanol-induced cell death. The levels of reactive oxygen species production and loss of mitochondrial membrane potential (DeltaPsi(m)) were also determined to assess the effects of Chrysophanol. However, reductions in adenosine triphosphate levels and increases in lactate dehydrogenase activity indicated that Chrysophanol stimulated necrotic cell death. In summary, human liver cancer cells treated with Chrysophanol exhibited a cellular pattern associated with necrosis and not apoptosis.

Synergistic interaction of physcion and chrysophanol on plant powdery mildew.[Pubmed:17397111]

Pest Manag Sci. 2007 May;63(5):511-5.

The extract of the plant Rheum officinale Baill, mainly containing the anthraquinones physcion and Chrysophanol, is highly active against plant powdery mildew. Experiments were conducted in the laboratory and greenhouse to determine the interaction of the two compounds on cucumber powdery mildew [Sphaerotheca fuliginea (Schlecht.) Poll] and on wheat powdery mildew [Blumeria graminis (DC.) Speer f. sp. tritici Marchal]. Physcion was much more bioactive than Chrysophanol against these powdery mildews. There was a significant synergistic interaction between the two compounds on the diseases when the ratios of physcion to Chrysophanol ranged from 1:9 to 5:5. The synergistic degree increased with increase in the Chrysophanol proportion in the combination. The findings indicate that, in order to ensure constant efficacy of the extract on the disease, both the contents and the proportion of the main active ingredients physcion and Chrysophanol have to be determined.

Chrysophanol-induced cell death (necrosis) in human lung cancer A549 cells is mediated through increasing reactive oxygen species and decreasing the level of mitochondrial membrane potential.[Pubmed:22848001]

Environ Toxicol. 2014 May;29(7):740-9.

Chrysophanol (1,8-dihydroxy-3-methylanthraquinone) is one of the anthraquinone compounds, and it has been shown to induce cell death in different types of cancer cells. The effects of Chrysophanol on human lung cancer cell death have not been well studied. The purpose of this study is to examine Chrysophanol-induced cytotoxic effects and also to investigate such influences that involved apoptosis or necrosis in A549 human lung cancer cells in vitro. Our results indicated that Chrysophanol decreased the viable A549 cells in a dose- and time-dependent manner. Chrysophanol also promoted the release of reactive oxygen species (ROS) and Ca(2+) and decreased the levels of mitochondria membrane potential (DeltaPsim ) and adenosine triphosphate in A549 cells. Furthermore, Chrysophanol triggered DNA damage by using Comet assay and DAPI staining. Importantly, Chrysophanol only stimulated the cytocheome c release, but it did not activate other apoptosis-associated protein levels including caspase-3, caspase-8, Apaf-1, and AIF. In conclusion, human lung cancer A549 cells treated with Chrysophanol exhibited a cellular pattern associated with necrotic cell death and not apoptosis in vitro. (c) 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 740-749, 2014.

Description

Chrysophanol (Chrysophanic acid) is a natural anthraquinone, which inhibits EGF-induced phosphorylation of EGFR and suppresses activation of AKT and mTOR/p70S6K.

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