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6,7-Dihydroxycoumarin

CAS# 305-01-1

6,7-Dihydroxycoumarin

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Quality Control of 6,7-Dihydroxycoumarin

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Chemical structure

6,7-Dihydroxycoumarin

3D structure

Chemical Properties of 6,7-Dihydroxycoumarin

Cas No. 305-01-1 SDF Download SDF
PubChem ID 5281416 Appearance White-pale yellow powder
Formula C9H6O4 M.Wt 178.14
Type of Compound Coumarins Storage Desiccate at -20°C
Synonyms Aesculetin; Cichorigenin; Cichoriin aglycone; 6,7-Dihydroxycoumarin; Esculetol; Esculin aglycone
Solubility DMSO : 250 mg/mL (1403.39 mM; Need ultrasonic)
Chemical Name 6,7-dihydroxychromen-2-one
SMILES C1=CC(=O)OC2=CC(=C(C=C21)O)O
Standard InChIKey ILEDWLMCKZNDJK-UHFFFAOYSA-N
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 6,7-Dihydroxycoumarin

The peel of Aesculus hippocastanum L.

Biological Activity of 6,7-Dihydroxycoumarin

Description6,7-Dihydroxycoumarin(Esculetin) has various biological and pharmaceutical properties including anti-edema, anti-inflammatory, anti-tumour, hepatoprotective, anti-osteoarthritis and anti-rheumatoid arthritis effects. It inhibits lipoxygenases (LOs), p42/44 MAPK activation, PI3-kinase activation, as well as NF-kappaB and AP-1 activation, it exhibits competitive inhibition against the oxidation of 3-(3,4-dihydroxyphenyl)- alanine by mushroom, the IC50 value of is 43 microM.
TargetsHO-1 | NO | AP-1 | MCP-1 | TNF-α | PPAR | NF-kB | PI3K
In vitro

Esculetin (6,7-dihydroxycoumarin): a potential cancer chemopreventive agent through suppression of Sp1 in oral squamous cancer cells.[Pubmed: 25310400]

Int J Oncol. 2015 Jan;46(1):265-71.

Esculetin (6,7-Dihydroxycoumarin), a coumarin compound, is known to inhibit proliferation and induce apoptosis in several types of human cancer cells and is regarded as a promising chemotherapeutic agent.
METHODS AND RESULTS:
The purpose of the present study was to investigate the anti-proliferative effects of esculetin on two oral squamous cell carcinoma (OSCC) cell lines, HN22 and HSC4, through regulation of specificity protein 1 (Sp1). We examined the apoptotic effects of esculetin were measured by MTS assay, DAPI staining, Annexin V, PI staining, RT-PCR, western blot analysis and immunocytochemistry in HN22 and HSC4 cells. Taken together, the results of the present study indicate that esculetin had anti-proliferative effect on the growth of OSCC cells (HN22 and HSC4) in a dose- and time-dependent manner. The treatment of HN22 and HSC4 cells with esculetin led to a significant reduction in growth and induced apoptosis, followed by the regulation of Sp1 and Sp1 regulatory protein.
CONCLUSIONS:
This indicates that esculetin inhibited cell growth and induced apoptosis by suppressing Sp1 in HN22 and HSC4 cells, suggesting it to be a potent anticancer drug candidate for oral cancer.

Esculetin inhibits the inflammatory response by inducing heme oxygenase-1 in cocultured macrophages and adipocytes.[Pubmed: 25088305]

Food Funct. 2014 Sep;5(9):2371-7.


METHODS AND RESULTS:
In this study, we investigated the anti-inflammatory effects of esculetin (6,7-Dihydroxycoumarin,ECT) through up-regulation of heme oxygenase-1 (HO-1) in cocultured macrophages and adipocytes. RAW264.7 macrophages and differentiated 3T3-L1 adipocytes were cocultured in serum-free Dulbecco's modified Eagle's medium with or without ECT for 24 h. Nitric oxide (NO), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) production was measured in the coculture supernatant. ECT decreased the secretion of NO, TNF-α, and MCP-1. The expression of adipogenic proteins, including peroxisome proliferator-activated receptors γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα) in cocultured adipocytes and inducible nitric oxide synthase (iNOS) in cocultured macrophages, was inhibited by ECT. Additionally, HO-1 expression was induced in cocultured macrophages and adipocytes. Silencing of HO-1 expression increased the production of NO, TNF-α, and MCP-1 in cocultured cells, in spite of the presence of ECT.
CONCLUSIONS:
This study demonstrated that ECT exhibited anti-inflammatory properties by inhibiting the production of proinflammatory cytokines in the interaction between adipocytes and macrophages through HO-1 expression. ECT may have the potential to improve chronic inflammation in obesity.

Esculetin suppresses proteoglycan metabolism by inhibiting the production of matrix metalloproteinases in rabbit chondrocytes.[Pubmed: 10334506]

Eur. J. Pharmacol., 1999, 370(3):297-305

The possible mechanism of the chondroprotective effect of 6,7-Dihydroxycoumarin (esculetin) was investigated using primary cultures of rabbit articular chondrocytes.
METHODS AND RESULTS:
Esculetin (EST) significantly suppressed the proteoglycan depletion and the release of pulse-labeled [35S]proteoglycan from the matrix layer of rabbit chondrocytes treated with recombinant human interleukin-1alpha. The matrix metalloproteinase inhibitor, 1,10-phenanthroline, also blocked the proteoglycan depletion and [35S]proteoglycan release. From these results, it is likely that recombinant human interleukin-1alpha-induced proteoglycan depletion is mediated by matrix metalloproteinases. Although esculetin did not directly inhibit collagenolytic activity in the culture media, it significantly suppressed the production of pro-matrix metalloproteinase-1/interstitial procollagenase and pro-matrix metalloproteinase-3/prostromelysin 1, accompanied by a decrease in the steady-state levels of their mRNAs.
CONCLUSIONS:
These results suggest that esculetin is a therapeutically effective candidate for inhibition of cartilage destruction in osteoarthritis and rheumatoid arthritis.

Protocol of 6,7-Dihydroxycoumarin

Kinase Assay

Mushroom tyrosinase inhibitory activity of esculetin isolated from seeds of Euphorbia lathyris L.[Pubmed: 12723615 ]

Esculetin inhibits Ras-mediated cell proliferation and attenuates vascular restenosis following angioplasty in rats.[Pubmed: 12781342]

Biochem Pharmacol. 2003 Jun 1;65(11):1897-905.

The proliferation of vascular smooth muscle cells (VSMCs) induced by injury to the intima of arteries is an important etiologic factor in vascular proliferative disorders such as atherosclerosis and restenosis. Esculetin, derived from the Chinese herb Artemisia scoparia, is well known as a lipoxygenase inhibitor.
METHODS AND RESULTS:
We have investigated the inhibitory effects of esculetin (6,7-Dihydroxycoumarin) on VSMC proliferation and intimal hyperplasia by balloon angioplasty in the rat. We determined, using [3H]thymidine incorporation and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, that esculetin inhibited the proliferation of VSMCs via a lipoxygenase-independent pathway. Three predominant signaling pathways were identified to be inhibited by esculetin: (a) the activation of p42/44 mitogen-activated protein kinase (MAPK) and the downstream effectors of c-fos and c-jun immediate early genes by means of western and reverse transcription-polymerase chain reaction (RT-PCR) analyses; (b) the activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1), using the electrophoretic mobility shift assay; and (c) the activation of phosphoinositide 3-kinase (PI 3-kinase) and cell cycle progression, by western blot analysis and flow cytometric detection. Furthermore, esculetin also profoundly inhibited Ras activation, a shared upstream event of the above signaling cascades. In vascular injury studies, intraperitoneal administration of esculetin significantly suppressed intimal hyperplasia induced by balloon angioplasty.
CONCLUSIONS:
We conclude that esculetin blocks cell proliferation via the inhibition of an upstream effector of Ras and downstream events including p42/44 MAPK activation, PI 3-kinase activation, immediate early gene expression, as well as NF-kappaB and AP-1 activation. It also inhibits intimal hyperplasia after balloon vascular injury in the rat, indicating the therapeutic potential for treating restenosis after arterial injury.

Biosci Biotechnol Biochem. 2003 Mar;67(3):631-4.

A tyrosinase inhibitor was isolated from the seeds of Euphorbia lathyris L. by bioassay-guided fractionation and purification, using silica gel column chromatography. It was identified as esculetin (6,7-Dihydroxycoumarin)by comparing its physical properties and spectral data with those of an authentic sample. The IC50 value of esculetin(6,7-Dihydroxycoumarin) in the mushroom tyrosinase activity test was 43 microM. The kinetic study indicates that esculetin(6,7-Dihydroxycoumarin) exhibited competitive inhibition against the oxidation of 3-(3,4-dihydroxyphenyl)-alanine by mushroom tyrosinase. The structure-activity relationships among five esculetin(6,7-Dihydroxycoumarin) analogs suggest that hydroxyl groups at the C6 and C7 positions of the coumarin skeleton played an important role in the expression of tyrosinase inhibitory activity.

Cell Research

Esculetin induces apoptosis and inhibits adipogenesis in 3T3-L1 cells.[Pubmed: 17062797 ]

Obesity (Silver Spring). 2006 Oct;14(10):1691-9.

Cell lines:3T3-L1 mouse embryo fibroblasts
Concentrations: 0, 50, 100, 200, 400, 800 μM
Incubation Time: 6, 12, 24, or 48 hours
Method:
Tests are performed in 96-well plates. For mature adipocytes, cells are seeded (5000 cells/well), grown to confluency, induced to differentiate, and grown to maturation. For preadipocytes, a seeding density of 2500 cells/well is used, and cells are cultured overnight before treatment. Cells are incubated with either DMSO or increasing concentrations of esculetin for 6, 12, 24, or 48 hours. For the post-confluent preadipocytes, a seeding density of 2500 cells/well is used, and cells are grown to confluency before treatment. Esculetin (100 or 200 μM) in 0.01% DMSO carrier is added with the induction medium for Days 0 to 2, 2 to 4, and 4 to 6 of adipogenesis. Medium is changed every 2 days. Before assay for cell viability, cells are washed with DMEM/10% FBS three times, and 100 μL of DMEM/10% FBS medium is added to each well before treatment with 20 μL MTS assay solution per well. Cells are incubated for 1 hour at 37 °C; then 25 μL of 10% sodium dodecyl sulfate is added to each well. The absorbance is measured at 490 nm in a plate reader to determine the formazan concentration, which is proportional to the number of live cells.

Animal Research

Esculetin(6,7-Dihydroxycoumarin), a coumarin derivative, exerts in vitro and in vivo antiproliferative activity against hepatocellular carcinoma by initiating a mitochondrial-dependent apoptosis pathway.[Pubmed: 25517918 ]

Braz J Med Biol Res. 2015 Mar;48(3):245-53.

Animal Models: C57BL/6J mice implanted with Hepa1-6 cells
Formulation: physiological saline
Dosages:200, 400, or 700 mg/kg/day
Administration: i.p.

6,7-Dihydroxycoumarin Dilution Calculator

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Preparing Stock Solutions of 6,7-Dihydroxycoumarin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 5.6136 mL 28.0678 mL 56.1356 mL 112.2712 mL 140.3391 mL
5 mM 1.1227 mL 5.6136 mL 11.2271 mL 22.4542 mL 28.0678 mL
10 mM 0.5614 mL 2.8068 mL 5.6136 mL 11.2271 mL 14.0339 mL
50 mM 0.1123 mL 0.5614 mL 1.1227 mL 2.2454 mL 2.8068 mL
100 mM 0.0561 mL 0.2807 mL 0.5614 mL 1.1227 mL 1.4034 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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References on 6,7-Dihydroxycoumarin

Esculetin suppresses proteoglycan metabolism by inhibiting the production of matrix metalloproteinases in rabbit chondrocytes.[Pubmed:10334506]

Eur J Pharmacol. 1999 Apr 16;370(3):297-305.

The possible mechanism of the chondroprotective effect of 6,7-Dihydroxycoumarin (esculetin) was investigated using primary cultures of rabbit articular chondrocytes. Esculetin (EST) significantly suppressed the proteoglycan depletion and the release of pulse-labeled [35S]proteoglycan from the matrix layer of rabbit chondrocytes treated with recombinant human interleukin-1alpha. The matrix metalloproteinase inhibitor, 1,10-phenanthroline, also blocked the proteoglycan depletion and [35S]proteoglycan release. From these results, it is likely that recombinant human interleukin-1alpha-induced proteoglycan depletion is mediated by matrix metalloproteinases. Although esculetin did not directly inhibit collagenolytic activity in the culture media, it significantly suppressed the production of pro-matrix metalloproteinase-1/interstitial procollagenase and pro-matrix metalloproteinase-3/prostromelysin 1, accompanied by a decrease in the steady-state levels of their mRNAs. These results suggest that esculetin is a therapeutically effective candidate for inhibition of cartilage destruction in osteoarthritis and rheumatoid arthritis.

Esculetin (6,7-dihydroxycoumarin): a potential cancer chemopreventive agent through suppression of Sp1 in oral squamous cancer cells.[Pubmed:25310400]

Int J Oncol. 2015 Jan;46(1):265-71.

Esculetin (6,7-Dihydroxycoumarin), a coumarin compound, is known to inhibit proliferation and induce apoptosis in several types of human cancer cells and is regarded as a promising chemotherapeutic agent. The purpose of the present study was to investigate the anti-proliferative effects of esculetin on two oral squamous cell carcinoma (OSCC) cell lines, HN22 and HSC4, through regulation of specificity protein 1 (Sp1). We examined the apoptotic effects of esculetin were measured by MTS assay, DAPI staining, Annexin V, PI staining, RT-PCR, western blot analysis and immunocytochemistry in HN22 and HSC4 cells. Taken together, the results of the present study indicate that esculetin had anti-proliferative effect on the growth of OSCC cells (HN22 and HSC4) in a dose- and time-dependent manner. The treatment of HN22 and HSC4 cells with esculetin led to a significant reduction in growth and induced apoptosis, followed by the regulation of Sp1 and Sp1 regulatory protein. This indicates that esculetin inhibited cell growth and induced apoptosis by suppressing Sp1 in HN22 and HSC4 cells, suggesting it to be a potent anticancer drug candidate for oral cancer.

Esculetin inhibits the inflammatory response by inducing heme oxygenase-1 in cocultured macrophages and adipocytes.[Pubmed:25088305]

Food Funct. 2014 Sep;5(9):2371-7.

Obesity is associated with chronic low-grade inflammation of adipose tissue. In this study, we investigated the anti-inflammatory effects of esculetin (ECT) through up-regulation of heme oxygenase-1 (HO-1) in cocultured macrophages and adipocytes. RAW264.7 macrophages and differentiated 3T3-L1 adipocytes were cocultured in serum-free Dulbecco's modified Eagle's medium with or without ECT for 24 h. Nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), and monocyte chemoattractant protein-1 (MCP-1) production was measured in the coculture supernatant. ECT decreased the secretion of NO, TNF-alpha, and MCP-1. The expression of adipogenic proteins, including peroxisome proliferator-activated receptors gamma (PPARgamma) and CCAAT/enhancer binding protein alpha (C/EBPalpha) in cocultured adipocytes and inducible nitric oxide synthase (iNOS) in cocultured macrophages, was inhibited by ECT. Additionally, HO-1 expression was induced in cocultured macrophages and adipocytes. Silencing of HO-1 expression increased the production of NO, TNF-alpha, and MCP-1 in cocultured cells, in spite of the presence of ECT. This study demonstrated that ECT exhibited anti-inflammatory properties by inhibiting the production of proinflammatory cytokines in the interaction between adipocytes and macrophages through HO-1 expression. ECT may have the potential to improve chronic inflammation in obesity.

Esculetin inhibits Ras-mediated cell proliferation and attenuates vascular restenosis following angioplasty in rats.[Pubmed:12781342]

Biochem Pharmacol. 2003 Jun 1;65(11):1897-905.

The proliferation of vascular smooth muscle cells (VSMCs) induced by injury to the intima of arteries is an important etiologic factor in vascular proliferative disorders such as atherosclerosis and restenosis. Esculetin, derived from the Chinese herb Artemisia scoparia, is well known as a lipoxygenase inhibitor. We have investigated the inhibitory effects of esculetin on VSMC proliferation and intimal hyperplasia by balloon angioplasty in the rat. We determined, using [3H]thymidine incorporation and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, that esculetin inhibited the proliferation of VSMCs via a lipoxygenase-independent pathway. Three predominant signaling pathways were identified to be inhibited by esculetin: (a) the activation of p42/44 mitogen-activated protein kinase (MAPK) and the downstream effectors of c-fos and c-jun immediate early genes by means of western and reverse transcription-polymerase chain reaction (RT-PCR) analyses; (b) the activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1), using the electrophoretic mobility shift assay; and (c) the activation of phosphoinositide 3-kinase (PI 3-kinase) and cell cycle progression, by western blot analysis and flow cytometric detection. Furthermore, esculetin also profoundly inhibited Ras activation, a shared upstream event of the above signaling cascades. In vascular injury studies, intraperitoneal administration of esculetin significantly suppressed intimal hyperplasia induced by balloon angioplasty. We conclude that esculetin blocks cell proliferation via the inhibition of an upstream effector of Ras and downstream events including p42/44 MAPK activation, PI 3-kinase activation, immediate early gene expression, as well as NF-kappaB and AP-1 activation. It also inhibits intimal hyperplasia after balloon vascular injury in the rat, indicating the therapeutic potential for treating restenosis after arterial injury.

Esculetin induces apoptosis and inhibits adipogenesis in 3T3-L1 cells.[Pubmed:17062797]

Obesity (Silver Spring). 2006 Oct;14(10):1691-9.

OBJECTIVE: To determine the effects of esculetin, a plant phenolic compound with apoptotic activity in cancer cells, on 3T3-L1 adipocyte apoptosis and adipogenesis. RESEARCH METHODS AND PROCEDURES: 3T3-L1 pre-confluent preadipocytes and lipid-filled adipocytes were incubated with esculetin (0 to 800 microM) for up to 48 hours. Viability was determined using the Cell Titer 96 Aqueous One Solution cell proliferation assay; apoptosis was quantified by measurement of single-stranded DNA. Post-confluent preadipocytes were incubated with esculetin for up to 6 days during maturation. Adipogenesis was quantified by measuring lipid content using Nile Red dye; cells were also stained with Oil Red O for visual confirmation of effects on lipid accumulation. RESULTS: In mature adipocytes, esculetin caused a time- and dose-related increase in adipocyte apoptosis and a decrease in viability. Apoptosis was increased after only 6 hours by 400 and 800 microM esculetin (p < 0.05), and after 48 hours, as little as 50 microM esculetin increased apoptosis (p < 0.05). In preadipocytes, apoptosis was detectable only after 48 hours (p < 0.05) with 200 microM esculetin and higher concentrations. However, results of the cell viability assay indicated a reduction in preadipocyte number in a time- and dose-related manner, beginning as early as 6 hours with 400 and 800 microM esculetin (p < 0.05). Esculetin also inhibited adipogenesis of 3T3-L1 preadipocytes. Esculetin-mediated inhibition of adipocyte differentiation occurred during the early, intermediate, and late stages of the differentiation process. In addition, esculetin induced apoptosis during the late stage of differentiation. DISCUSSION: These findings suggest that esculetin can alter fat cell number by direct effects on cell viability, adipogenesis, and apoptosis in 3T3-L1 cells.

Inhibitory effect of esculetin on oxidative damage induced by t-butyl hydroperoxide in rat liver.[Pubmed:11097384]

Arch Toxicol. 2000 Oct;74(8):467-72.

Increasing evidence regarding free radical-generating agents and inflammatory processes suggests that accumulation of reactive oxygen species can cause hepatotoxicity. A short-chain analog of lipid hydroperoxide, t-butyl hydroperoxide (t-BHP), can be metabolized to free radical intermediates by cytochrome P-450 in hepatocytes, which in turn can initiate lipid peroxidation, affect cell integrity and result in cell injury. In this study, we used t-BHP to induce hepatotoxicity in vitro and in vivo and determined the antioxidative bioactivity of esculetin, a coumarin compound. Our investigations showed that pretreatment with esculetin (5-20 microg/ml) significantly decreased the leakage of lactate dehydrogenase (LDH) and alanine transaminase (ALT), and also decreased the formation of malondialdehyde (MDA) in primary cultured rat hepatocytes induced by a 30-min treatment with t-BHP. An in vivo study in rats showed that pretreatment with esculetin (i.p.) at concentrations of 0.5 and 5 mg/kg for 5 days before a single i.p. dose of t-BHP (0.1 mmol/kg) significantly lowered the serum levels of the hepatic enzyme markers (ALT and AST) and reduced oxidative stress in the liver. Histopathological evaluation of the rat livers revealed that esculetin reduced the incidence of liver lesions induced by t-BHP, including hepatocyte swelling, leukocyte infiltration, and necrosis. Based on the results described above, we speculate that esculetin may play a chemopreventive role via reducing oxidative stress in living systems.

Mushroom tyrosinase inhibitory activity of esculetin isolated from seeds of Euphorbia lathyris L.[Pubmed:12723615]

Biosci Biotechnol Biochem. 2003 Mar;67(3):631-4.

A tyrosinase inhibitor was isolated from the seeds of Euphorbia lathyris L. by bioassay-guided fractionation and purification, using silica gel column chromatography. It was identified as esculetin by comparing its physical properties and spectral data with those of an authentic sample. The IC50 value of esculetin in the mushroom tyrosinase activity test was 43 microM. The kinetic study indicates that esculetin exhibited competitive inhibition against the oxidation of 3-(3,4-dihydroxyphenyl)-alanine by mushroom tyrosinase. The structure-activity relationships among five esculetin analogs suggest that hydroxyl groups at the C6 and C7 positions of the coumarin skeleton played an important role in the expression of tyrosinase inhibitory activity.

Description

Esculetin is an active ingredient extracted mainly from the bark of Fraxinus rhynchophylla. Esculetin inhibits platelet-derived growth factor (PDGF)-induced airway smooth muscle cells (ASMCs) phenotype switching through inhibition of PI3K/Akt pathway. Esculetin has antioxidant, antiinflammatory, and antitumor activities.

Keywords:

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