Farrerol

CAS# 24211-30-1

Farrerol

Catalog No. BCN2481----Order now to get a substantial discount!

Product Name & Size Price Stock
Farrerol: 5mg $12 In Stock
Farrerol: 10mg Please Inquire In Stock
Farrerol: 20mg Please Inquire Please Inquire
Farrerol: 50mg Please Inquire Please Inquire
Farrerol: 100mg Please Inquire Please Inquire
Farrerol: 200mg Please Inquire Please Inquire
Farrerol: 500mg Please Inquire Please Inquire
Farrerol: 1000mg Please Inquire Please Inquire

Quality Control of Farrerol

Number of papers citing our products

Chemical structure

Farrerol

3D structure

Chemical Properties of Farrerol

Cas No. 24211-30-1 SDF Download SDF
PubChem ID 442396 Appearance White powder
Formula C17H16O5 M.Wt 300.3
Type of Compound Flavonoids Storage Desiccate at -20°C
Synonyms 4',5,7-Trihydroxy 6,8-dimethylflavanone
Solubility Soluble in ethanol and methan
Chemical Name (2S)-5,7-dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethyl-2,3-dihydrochromen-4-one
SMILES CC1=C(C2=C(C(=C1O)C)OC(CC2=O)C3=CC=C(C=C3)O)O
Standard InChIKey DYHOLQACRGJEHX-ZDUSSCGKSA-N
Standard InChI InChI=1S/C17H16O5/c1-8-15(20)9(2)17-14(16(8)21)12(19)7-13(22-17)10-3-5-11(18)6-4-10/h3-6,13,18,20-21H,7H2,1-2H3/t13-/m0/s1
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 Farrerol

1 Sterculia sp.

Biological Activity of Farrerol

DescriptionFarrerol has antioxidative, anti-bacterial, anti-inflammatory, antiangiogenic activities, it is a potential candidate for the intervention of endothelial-injury-associated cardiovascular diseases. Farrerol inactivates KEAP-1 or activates the Akt, p38 and ERK to facilitate the release of Nrf2 from Keap1 and subsequent reduces the intracellular production of reactive oxygen species via the induction of HO-1 expression. Farrerol can inhibit angiogenesis through down regulation of Akt/mTOR, Erk and Jak2/Stat3 signal pathway, and can inhibit IL-1β-induced inflammatory responses in osteoarthritis chondrocytes by blocking PI3K/Akt/NF-κB signaling pathway.
TargetsHO-1 | ROS | Akt | p38MAPK | JNK | ERK | Nrf2 | Bcl-2/Bax | Caspase | NO | NF-kB | SOD | PGE | IL Receptor | PI3K | mTOR | JAK | STAT
In vitro

The antioxidative potential of farrerol occurs via the activation of Nrf2 mediated HO-1 signaling in RAW 264.7 cells.[Pubmed: 26111761]

Chem Biol Interact. 2015 Jun 22.

Farrerol, (S)-2,3-dihydro-5,7-dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethyl-4-benzopyrone, isolated from rhododendron, has been shown to have antioxidative potential, but the molecular mechanism underlying this activity remains unclear. The inducible expression of heme oxygenase-1 (HO-1), a potent antioxidative and cytoprotective enzyme, is known to play an important role in cytoprotection in a variety of pathological models.
METHODS AND RESULTS:
In this study, we evaluated the antioxidative potential of Farrerol against oxidative damage and investigated its antioxidative mechanism in RAW 264.7 cells. The molecular mechanism underlying the cytoprotective function of Farrerol was determined by analyzing intracellular signaling pathways, transcriptional activation and the inhibitory effect of HO-1 on ROS production. Farrerol induced antioxidant enzymes mRNA expression, HO-1 protein expression and nuclear translocation of NF-E2-related factor 2 in RAW 264.7 macrophage cells. Farrerol down-regulated the expression of the Keap1 protein and the thiol reducing agents attenuated Farrerol-induced HO-1 expression. Further investigation utilizing Western blotting and specific inhibitors of Akt, p38, JNK and ERK demonstrated that Akt, p38, and ERK axis of signaling pathway mediates HO-1 expression. Moreover, tert-butyl hydroperoxide (t-BHP)-induced oxidative damage was ameliorated by Farrerol treatment in a dose-dependent manner, which was abolished by Akt, p38, ERK and HO-1 inhibitors (Snpp). It is hence likely that Farrerol inactivated KEAP-1 or activated the Akt, p38 and ERK to facilitate the release of Nrf2 from Keap1 and subsequent reduced the intracellular production of reactive oxygen species via the induction of HO-1 expression.
CONCLUSIONS:
These results support the central role of HO-1 in the cytoprotective effect of Farrerol.

Farrerol regulates antimicrobial peptide expression and reduces Staphylococcus aureus internalization into bovine mammary epithelial cells.[Pubmed: 24036182]

Microb Pathog. 2013 Dec;65:1-6.

Mastitis, defined as inflammation of the mammary gland, is an infectious disease with a major economic influence on dairy industry. Staphylococcus aureus is a common gram-positive pathogen that frequently causes subclinical, chronic infection of the mammary gland in dairy cows. Farrerol, a traditional Chinese medicine isolated from rhododendron, has been shown to have anti-bacterial activity. However, the effect of Farrerol on S. aureus infection in mammary epithelium has not been studied in detail. The aim of this study was to investigate the effect of Farrerol on the invasion of bovine mammary epithelial cells (bMEC) by S. aureus.
METHODS AND RESULTS:
The expression of antimicrobial peptide genes by bMEC were assessed in the presence or absence of S. aureus infection. Our results demonstrated that Farrerol (4-16 μg/ml) reduced > 55% the internalization of S. aureus into bMEC. We also found that Farrerol was able to down-regulate the mRNA expression of tracheal antimicrobial peptide (TAP) and bovine neutrophil β-defensin 5 (BNBD5) in bMEC infected with S. aureus. The Nitric oxide (NO) production of bMEC after S. aureus stimulation was decreased by Farrerol treatment. Furthermore, Farrerol treatment suppressed S. aureus-induced NF-κB activation in bMEC.
CONCLUSIONS:
These results demonstrated that Farrerol modulated TAP and BNBD5 gene expression in mammary gland, enhances bMEC defense against S. aureus infection and could be useful in protection against bovine mastitis.

Anti-inflammatory effects of farrerol on IL-1β-stimulated human osteoarthritis chondrocytes.[Pubmed: 26162701 ]

Eur J Pharmacol. 2015 Oct 5;764:443-7.

The present study aimed to investigate the anti-inflammatory effects and the underlying molecular mechanism of Farrerol on IL-1β-stimulated human osteoarthritis chondrocytes.
METHODS AND RESULTS:
Chondrocytes were pretreated with Farrerol 1h before IL-1β stimulation. The effects of Farrerol on NO and PGE2 production were tested by Griess reagent and ELISA. The effects of Farrerol on COX-2, iNOS, Akt, phosphorylated Akt, and NF-κB activation were measured by western blot analysis. The results showed that Farrerol remarkably inhibited IL-1β-induced NO and PGE2 production, as well as COX-2 and iNOS expression. Farrerol also inhibited IL-1β-induced NF-κB activation. Furthermore, Farrerol significantly inhibited IL-1β-induced phosphorylation of PI3K and Akt.
CONCLUSIONS:
In conclusion, these results indicated that Farrerol inhibited IL-1β-induced inflammatory responses in osteoarthritis chondrocytes by blocking PI3K/Akt/NF-κB signaling pathway.

Protocol of Farrerol

Kinase Assay

Farrerol regulates occludin expression in hydrogen peroxide-induced EA.hy926 cells by modulating ERK1/2 activity.[Pubmed: 24726849]

Apoptosis induced by farrerol in human gastric cancer SGC-7901 cells through the mitochondrial-mediated pathway.[Pubmed: 26061993]

Eur J Cancer Prev. 2015 Jun 5.

Farrerol, a typical flavanone isolated from the Chinese medicinal plant Rhododendron dauricum L., has been found to show various biological activities. However, to the best of our knowledge, its inhibitory actions against cancer cells have not been reported as yet.
METHODS AND RESULTS:
Therefore, the present study aimed to investigate the cytotoxic and apoptotic effects of Farrerol on human gastric cancer SGC-7901 cells. Farrerol showed a 50% inhibition of SGC-7901 cell growth at a concentration of 40.4 μmol/l for 24 h according to MTT assays. The cell morphology results indicated that SGC-7901 cells treated with Farrerol showed several features of apoptotic cell death, which was also confirmed by the Annexin-V FITC/PI double-staining assay. Further studies showed that Farrerol treatment induced the attenuation of mitochondrial membrane potential, accompanied by the release of Cyt-c and the activation of caspase-9 and caspase-3. Furthermore, Farrerol decreased the gene expression of Bcl-2, whereas the gene expression level of Bax was found to increase after Farrerol treatment.
CONCLUSIONS:
These combined results indicated that Farrerol can induce apoptosis through a mitochondrial-mediated pathway.

Eur J Pharmacol. 2014 Jul 5;734:9-14.

Endothelial tight junction is a crucial intracellular junctional structure that controls paracellular permeability across vascular endothelium. Oxidative stress-mediated elevation in endothelial permeability is associated with pathogenesis of several cardiovascular diseases.
METHODS AND RESULTS:
In the present research, the regulation of Farrerol on occludin, a transmembrane proteins associated with endothelial tight junction, was investigated in hydrogen peroxide-induced human endothelium-derived EA.hy926 cells. Western blot analysis demonstrated that H2O2 exposure caused a significant decrease in occludin expression, but had little effect on ZO-1 expression, and the decrease of occludin expression was significantly attenuated by Farrerol in a dose-dependent manner. Meanwhile, immunofluorescent staining assay also demonstrated that the loss of occludin expression induced by H2O2 exposure was restored by Farrerol pretreatment. Further investigations showed that Farrerol prevented H2O2-induced activation of extracellular signal-regulated kinase (ERK) 1/2 in a dose-dependent manner. The use of U0126, a specific inhibitor of MEK1/2, proved that H2O2-induced decrease of occludin in EA.hy926 cells was likely associated with activation of ERK1/2, which indicated that the regulation of Farrerol on occludin expression in H2O2-induced EA.hy926 cells was likely related to the modulation of ERK1/2 activation.
CONCLUSIONS:
In conclusion, the present study demonstrates for the first time that Farrerol has potential effects on oxidative stress-induced endothelial tight junction disruption and suggests that Farrerol is a potential candidate for the intervention of endothelial permeability-associated cardiovascular diseases.

Cell Research

Farrerol inhibited angiogenesis through Akt/mTOR, Erk and Jak2/Stat3 signal pathway.[Pubmed: 27235707]

Protective effects of farrerol against hydrogen-peroxide-induced apoptosis in human endothelium-derived EA.hy926 cells.[Pubmed: 23984825]

Can J Physiol Pharmacol. 2013 Sep;91(9):733-40.

Vascular endothelium plays an important role in the physiological homeostasis of blood vessels. Endothelial injury is considered to be implicated in the pathogenesis of many cardiovascular diseases, including atherosclerosis. Farrerol, a flavonoid considered to be the major bioactive component in a traditional Chinese herb, "Man-shan-hong", which is the dried leaves of Rhododendron dauricum L., displays many bioactive properties, including antibechic, antibacterial, anti-inflammatory, and the inhibition of vascular smooth muscle cell (VSMC) proliferation.
METHODS AND RESULTS:
In this study, the protective effects of Farrerol on hydrogen peroxide (H2O2)-induced apoptosis in human endothelium-derived EA.hy926 cells were investigated. The results showed that Farrerol significantly inhibited the loss of cell viability and enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in H2O2-induced EA.hy926 cells. Meanwhile, Farrerol inhibited H2O2-induced elevation in the levels of intracellular malondialdehyde and reactive oxygen species, as well as cell apoptosis. Furthermore, real time RT-PCR and Western blot analysis showed that Farrerol significantly decreased the expression of Bax mRNA, Bax, cleaved caspase-3, and phosph-p38 MAPK, while increasing the exporession of Bcl-2 mRNA and Bcl-2 in H2O2-induced EA.hy926 cells.
CONCLUSIONS:
These results are the first demonstration that Farrerol has protective effects against H2O2-induced apoptosis in EA.hy926 cells, and suggests that Farrerol is a potential candidate for the intervention of endothelial-injury-associated cardiovascular diseases.

Phytomedicine. 2016 Jun 15;23(7):686-93.

Farrerol is one of traditional Chinese medicines, isolated from Rhododendron dauricum L. It has been reported that Farrerol exerts multiple biological activities. Angiogenesis is an important drug target for cancer and inflammation therapy, the effect of Farrerol on angiogenesis is unknown. We aimed to investigate whether Farrerol may have inhibitory effects against angiogenesis.
METHODS AND RESULTS:
Two kinds of endothelial cells, named human umbilical vein endothelia cell and human micro vessel endothelial cells, were used to examine the effect and mechanism of Farrerol on angiogenesis. MTT assay was used to detect cell proliferation, wound healing assay and boyden's chamber assay were used to examine cell migration, Matrigel was used as basement membrane substratum in tube formation assay, Annexin V-FITC/PI dual staining assay and trypan blue staining were used to detect cell apoptosis, mouse aortic rings assay was performed as ex vivo assay, the expression of proteins involved in angiogenesis was tested using western blot, the binding of Farrerol to Stat3 was monitored by docking assay, molecular dynamics simulations and MM-GBSA method. Farrerol showed an inhibitory effect on proliferation, migration and tube formation of human umbilical vein endothelia cell and human micro vessel endothelial cells in a concentration-dependent manner. Farrerol induced cell cycle arrest and increased the apoptotic percentage of endothelial cells. Farrerol also suppressed the formation of new micro vessels from mouse aortic rings. Moreover, Farrerol reduced the phosphorylation levels of Erk, Akt, mTOR, Jak2 and Stat3 as well as protein expression of Bcl-2 and Bcl-xl. Docking assay, molecular dynamics simulations and MM-GBSA method showed that Farrerol bound to domain of Stat3, Ser613,Gln635, Glu638 and Thr714 are the main residues in Farrerol binding sites with the binding free energy -7.3 ~ -9.0kcal/mol.
CONCLUSIONS:
In this study, we demonstrated that Farrerol inhibited angiogenesis through down regulation of Akt/mTOR, Erk and Jak2/Stat3 signal pathway. The inhibitory effect of Farrerol on angiogenesis suggested that this compound may be helpful to the angiogenesis-related diseases treatment, such as cancer and inflammations.

Farrerol Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Farrerol Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Farrerol

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.33 mL 16.65 mL 33.3 mL 66.6001 mL 83.2501 mL
5 mM 0.666 mL 3.33 mL 6.66 mL 13.32 mL 16.65 mL
10 mM 0.333 mL 1.665 mL 3.33 mL 6.66 mL 8.325 mL
50 mM 0.0666 mL 0.333 mL 0.666 mL 1.332 mL 1.665 mL
100 mM 0.0333 mL 0.1665 mL 0.333 mL 0.666 mL 0.8325 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.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University
Featured Products
New Products
 

References on Farrerol

The antioxidative potential of farrerol occurs via the activation of Nrf2 mediated HO-1 signaling in RAW 264.7 cells.[Pubmed:26111761]

Chem Biol Interact. 2015 Sep 5;239:192-9.

Farrerol, (S)-2,3-dihydro-5,7-dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethyl-4-benzopyrone, isolated from rhododendron, has been shown to have antioxidative potential, but the molecular mechanism underlying this activity remains unclear. The inducible expression of heme oxygenase-1 (HO-1), a potent antioxidative and cytoprotective enzyme, is known to play an important role in cytoprotection in a variety of pathological models. In this study, we evaluated the antioxidative potential of Farrerol against oxidative damage and investigated its antioxidative mechanism in RAW 264.7 cells. The molecular mechanism underlying the cytoprotective function of Farrerol was determined by analyzing intracellular signaling pathways, transcriptional activation and the inhibitory effect of HO-1 on ROS production. Farrerol induced antioxidant enzymes mRNA expression, HO-1 protein expression and nuclear translocation of NF-E2-related factor 2 in RAW 264.7 macrophage cells. Farrerol down-regulated the expression of the Keap1 protein and the thiol reducing agents attenuated Farrerol-induced HO-1 expression. Further investigation utilizing Western blotting and specific inhibitors of Akt, p38, JNK and ERK demonstrated that Akt, p38, and ERK axis of signaling pathway mediates HO-1 expression. Moreover, tert-butyl hydroperoxide (t-BHP)-induced oxidative damage was ameliorated by Farrerol treatment in a dose-dependent manner, which was abolished by Akt, p38, ERK and HO-1 inhibitors (Snpp). It is hence likely that Farrerol inactivated KEAP-1 or activated the Akt, p38 and ERK to facilitate the release of Nrf2 from Keap1 and subsequent reduced the intracellular production of reactive oxygen species via the induction of HO-1 expression. These results support the central role of HO-1 in the cytoprotective effect of Farrerol.

Anti-inflammatory effects of farrerol on IL-1beta-stimulated human osteoarthritis chondrocytes.[Pubmed:26162701]

Eur J Pharmacol. 2015 Oct 5;764:443-7.

The present study aimed to investigate the anti-inflammatory effects and the underlying molecular mechanism of Farrerol on IL-1beta-stimulated human osteoarthritis chondrocytes. Chondrocytes were pretreated with Farrerol 1h before IL-1beta stimulation. The effects of Farrerol on NO and PGE2 production were tested by Griess reagent and ELISA. The effects of Farrerol on COX-2, iNOS, Akt, phosphorylated Akt, and NF-kappaB activation were measured by western blot analysis. The results showed that Farrerol remarkably inhibited IL-1beta-induced NO and PGE2 production, as well as COX-2 and iNOS expression. Farrerol also inhibited IL-1beta-induced NF-kappaB activation. Furthermore, Farrerol significantly inhibited IL-1beta-induced phosphorylation of PI3K and Akt. In conclusion, these results indicated that Farrerol inhibited IL-1beta-induced inflammatory responses in osteoarthritis chondrocytes by blocking PI3K/Akt/NF-kappaB signaling pathway.

Farrerol regulates antimicrobial peptide expression and reduces Staphylococcus aureus internalization into bovine mammary epithelial cells.[Pubmed:24036182]

Microb Pathog. 2013 Dec;65:1-6.

Mastitis, defined as inflammation of the mammary gland, is an infectious disease with a major economic influence on dairy industry. Staphylococcus aureus is a common gram-positive pathogen that frequently causes subclinical, chronic infection of the mammary gland in dairy cows. Farrerol, a traditional Chinese medicine isolated from rhododendron, has been shown to have anti-bacterial activity. However, the effect of Farrerol on S. aureus infection in mammary epithelium has not been studied in detail. The aim of this study was to investigate the effect of Farrerol on the invasion of bovine mammary epithelial cells (bMEC) by S. aureus. The expression of antimicrobial peptide genes by bMEC were assessed in the presence or absence of S. aureus infection. Our results demonstrated that Farrerol (4-16 mug/ml) reduced > 55% the internalization of S. aureus into bMEC. We also found that Farrerol was able to down-regulate the mRNA expression of tracheal antimicrobial peptide (TAP) and bovine neutrophil beta-defensin 5 (BNBD5) in bMEC infected with S. aureus. The Nitric oxide (NO) production of bMEC after S. aureus stimulation was decreased by Farrerol treatment. Furthermore, Farrerol treatment suppressed S. aureus-induced NF-kappaB activation in bMEC. These results demonstrated that Farrerol modulated TAP and BNBD5 gene expression in mammary gland, enhances bMEC defense against S. aureus infection and could be useful in protection against bovine mastitis.

Protective effects of farrerol against hydrogen-peroxide-induced apoptosis in human endothelium-derived EA.hy926 cells.[Pubmed:23984825]

Can J Physiol Pharmacol. 2013 Sep;91(9):733-40.

Vascular endothelium plays an important role in the physiological homeostasis of blood vessels. Endothelial injury is considered to be implicated in the pathogenesis of many cardiovascular diseases, including atherosclerosis. Farrerol, a flavonoid considered to be the major bioactive component in a traditional Chinese herb, "Man-shan-hong", which is the dried leaves of Rhododendron dauricum L., displays many bioactive properties, including antibechic, antibacterial, anti-inflammatory, and the inhibition of vascular smooth muscle cell (VSMC) proliferation. In this study, the protective effects of Farrerol on hydrogen peroxide (H2O2)-induced apoptosis in human endothelium-derived EA.hy926 cells were investigated. The results showed that Farrerol significantly inhibited the loss of cell viability and enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in H2O2-induced EA.hy926 cells. Meanwhile, Farrerol inhibited H2O2-induced elevation in the levels of intracellular malondialdehyde and reactive oxygen species, as well as cell apoptosis. Furthermore, real time RT-PCR and Western blot analysis showed that Farrerol significantly decreased the expression of Bax mRNA, Bax, cleaved caspase-3, and phosph-p38 MAPK, while increasing the exporession of Bcl-2 mRNA and Bcl-2 in H2O2-induced EA.hy926 cells. These results are the first demonstration that Farrerol has protective effects against H2O2-induced apoptosis in EA.hy926 cells, and suggests that Farrerol is a potential candidate for the intervention of endothelial-injury-associated cardiovascular diseases.

Farrerol regulates occludin expression in hydrogen peroxide-induced EA.hy926 cells by modulating ERK1/2 activity.[Pubmed:24726849]

Eur J Pharmacol. 2014 Jul 5;734:9-14.

Endothelial tight junction is a crucial intracellular junctional structure that controls paracellular permeability across vascular endothelium. Oxidative stress-mediated elevation in endothelial permeability is associated with pathogenesis of several cardiovascular diseases. In the present research, the regulation of Farrerol on occludin, a transmembrane proteins associated with endothelial tight junction, was investigated in hydrogen peroxide-induced human endothelium-derived EA.hy926 cells. Western blot analysis demonstrated that H2O2 exposure caused a significant decrease in occludin expression, but had little effect on ZO-1 expression, and the decrease of occludin expression was significantly attenuated by Farrerol in a dose-dependent manner. Meanwhile, immunofluorescent staining assay also demonstrated that the loss of occludin expression induced by H2O2 exposure was restored by Farrerol pretreatment. Further investigations showed that Farrerol prevented H2O2-induced activation of extracellular signal-regulated kinase (ERK) 1/2 in a dose-dependent manner. The use of U0126, a specific inhibitor of MEK1/2, proved that H2O2-induced decrease of occludin in EA.hy926 cells was likely associated with activation of ERK1/2, which indicated that the regulation of Farrerol on occludin expression in H2O2-induced EA.hy926 cells was likely related to the modulation of ERK1/2 activation. In conclusion, the present study demonstrates for the first time that Farrerol has potential effects on oxidative stress-induced endothelial tight junction disruption and suggests that Farrerol is a potential candidate for the intervention of endothelial permeability-associated cardiovascular diseases.

Farrerol inhibited angiogenesis through Akt/mTOR, Erk and Jak2/Stat3 signal pathway.[Pubmed:27235707]

Phytomedicine. 2016 Jun 15;23(7):686-93.

BACKGROUND: Farrerol is one of traditional Chinese medicines, isolated from Rhododendron dauricum L. It has been reported that Farrerol exerts multiple biological activities. Angiogenesis is an important drug target for cancer and inflammation therapy, the effect of Farrerol on angiogenesis is unknown. HYPOTHESIS/PURPOSE: We aimed to investigate whether Farrerol may have inhibitory effects against angiogenesis. STUDY DESIGN/METHODS: Two kinds of endothelial cells, named human umbilical vein endothelia cell and human micro vessel endothelial cells, were used to examine the effect and mechanism of Farrerol on angiogenesis. MTT assay was used to detect cell proliferation, wound healing assay and boyden's chamber assay were used to examine cell migration, Matrigel was used as basement membrane substratum in tube formation assay, Annexin V-FITC/PI dual staining assay and trypan blue staining were used to detect cell apoptosis, mouse aortic rings assay was performed as ex vivo assay, the expression of proteins involved in angiogenesis was tested using western blot, the binding of Farrerol to Stat3 was monitored by docking assay, molecular dynamics simulations and MM-GBSA method. RESULTS: Farrerol showed an inhibitory effect on proliferation, migration and tube formation of human umbilical vein endothelia cell and human micro vessel endothelial cells in a concentration-dependent manner. Farrerol induced cell cycle arrest and increased the apoptotic percentage of endothelial cells. Farrerol also suppressed the formation of new micro vessels from mouse aortic rings. Moreover, Farrerol reduced the phosphorylation levels of Erk, Akt, mTOR, Jak2 and Stat3 as well as protein expression of Bcl-2 and Bcl-xl. Docking assay, molecular dynamics simulations and MM-GBSA method showed that Farrerol bound to domain of Stat3, Ser613,Gln635, Glu638 and Thr714 are the main residues in Farrerol binding sites with the binding free energy -7.3 approximately -9.0kcal/mol. CONCLUSIONS: In this study, we demonstrated that Farrerol inhibited angiogenesis through down regulation of Akt/mTOR, Erk and Jak2/Stat3 signal pathway. The inhibitory effect of Farrerol on angiogenesis suggested that this compound may be helpful to the angiogenesis-related diseases treatment, such as cancer and inflammations.

Apoptosis induced by farrerol in human gastric cancer SGC-7901 cells through the mitochondrial-mediated pathway.[Pubmed:26061993]

Eur J Cancer Prev. 2015 Sep;24(5):365-72.

Farrerol, a typical flavanone isolated from the Chinese medicinal plant Rhododendron dauricum L., has been found to show various biological activities. However, to the best of our knowledge, its inhibitory actions against cancer cells have not been reported as yet. Therefore, the present study aimed to investigate the cytotoxic and apoptotic effects of Farrerol on human gastric cancer SGC-7901 cells. Farrerol showed a 50% inhibition of SGC-7901 cell growth at a concentration of 40.4 mumol/l for 24 h according to MTT assays. The cell morphology results indicated that SGC-7901 cells treated with Farrerol showed several features of apoptotic cell death, which was also confirmed by the Annexin-V FITC/PI double-staining assay. Further studies showed that Farrerol treatment induced the attenuation of mitochondrial membrane potential, accompanied by the release of Cyt-c and the activation of caspase-9 and caspase-3. Furthermore, Farrerol decreased the gene expression of Bcl-2, whereas the gene expression level of Bax was found to increase after Farrerol treatment. These combined results indicated that Farrerol can induce apoptosis through a mitochondrial-mediated pathway.

Description

Farrerol is a bioactive constituent of Rhododendron, with broad activities such as anti-oxidative, anti-inflammatory, anti-tumor, neuroprotective and hepatoprotective effects.

Keywords:

Farrerol,24211-30-1,4',5,7-Trihydroxy 6,8-dimethylflavanone,Natural Products, buy Farrerol , Farrerol supplier , purchase Farrerol , Farrerol cost , Farrerol manufacturer , order Farrerol , high purity Farrerol

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: