Curcumol

CAS# 4871-97-0

Curcumol

Catalog No. BCN5976----Order now to get a substantial discount!

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Quality Control of Curcumol

Number of papers citing our products

Chemical structure

Curcumol

3D structure

Chemical Properties of Curcumol

Cas No. 4871-97-0 SDF Download SDF
PubChem ID 160771 Appearance White powder
Formula C15H24O2 M.Wt 236.35
Type of Compound Sesquiterpenes Storage Desiccate at -20°C
Synonyms (-)-Curcumol
Solubility DMSO : ≥ 100 mg/mL (423.10 mM)
H2O : < 0.1 mg/mL (insoluble)
*"≥" means soluble, but saturation unknown.
SMILES CC1CCC2C13CC(C(O3)(CC2=C)O)C(C)C
Standard InChIKey QRMPRVXWPCLVNI-XIQJJJERSA-N
Standard InChI InChI=1S/C15H24O2/c1-9(2)13-8-14-11(4)5-6-12(14)10(3)7-15(13,16)17-14/h9,11-13,16H,3,5-8H2,1-2,4H3/t11-,12-,13-,14?,15-/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 Curcumol

The rhizomes of Curcuma longa L.

Biological Activity of Curcumol

DescriptionCurcumol has antitumor, anti-inflammatory, and anti-seizure actions. It suppressed RANKL-induced osteoclast formation by attenuating the JNK signaling pathway, and inhibited Jak2-STAT signal pathway molecules of fibroblast-like synoviocytes in patients with rheumatoid arthritis. It is a novel anti-seizure agent which inhibited neuronal excitability through enhancing GABAergic inhibition.
TargetsCaspase | NF-kB | PI3K | JNK | AP-1 | TNF-α | IL Receptor | STAT | Bcl-2/Bax | IGF-1R | p38MAPK | PARP
In vitro

Curcumol induces HSC-T6 cell death through suppression of Bcl-2: involvement of PI3K and NF-κB pathways.[Pubmed: 25220584]

Eur J Pharm Sci. 2014 Dec 18;65:21-8.

The major feature in the molecular pathogenesis of hepatic fibrosis requires maintenance of the activated hepatic stellate cells (HSCs) phenotype by both proliferation and inhibition of apoptosis. Thus, the induction of activated HSCs apoptosis has been proposed as an antifibrotic treatment strategy. Curcumol has pro-apoptotic activity in a number of cancer cell types.
METHODS AND RESULTS:
The aim of this study is to test the hypothesis that the interruption of the phosphatidylinositol 3 kinase (PI3K)/nuclear factor-κB (NF-κB) signaling pathway by Curcumol might induce apoptosis of activated HSCs. Our results indicated that Curcumol-induced growth inhibition correlated with apoptosis induction as evidenced by Annexin V staining, and cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP) in HSC-T6. Importantly, we show that the apoptotic effect of Curcumol was specific to the activated HSCs (HSC-T6). Suppression of the NF-κB translocation via inhibition of IκB-α phosphorylation by the Curcumol led to the inhibition of expression of NF-κB-regulated gene, e.g. Bcl-xL and Bcl-2, in a PI3K-dependent manner, which is upstream of NF-κB activation. Also, Curcumol-mediated apoptosis of HSC-T6 were reversed by LY294002 and Bay 11-7082. Taken together, our findings perfectly support the hypothesis and demonstrate that the inhibition of PI3K/NF-κB pathway by Curcumol lead to HSC-T6 apoptosis.
CONCLUSIONS:
Thus, our study indicates that Curcumol is a potential candidate for further preclinical study aimed at the treatment of liver fibrosis.

Curcumol exhibits anti-inflammatory properties by interfering with the JNK-mediated AP-1 pathway in lipopolysaccharide-activated RAW264.7 cells.[Pubmed: 24269960]

Eur J Pharmacol. 2014 Jan 15;723:339-45.

Curcumol is one of the major components of the essential oil of Rhizoma Curcumae, a common traditional Chinese medicine with anti-inflammatory properties. However, the anti-inflammatory activity and the underlying molecular mechanisms of this compound remain unclear.
METHODS AND RESULTS:
In the present study, the anti-inflammation effect of Curcumol on lipopolysaccharide (LPS)-induced RAW264.7 cells is demonstrated along with its underlying mechanisms. We show that Curcumol inhibits LPS-induced NO production by suppressing iNOS mRNA expression and protein level but not iNOS activity. Moreover, Curcumol inhibits LPS-induced production of TNF-α, IL-1β and IL-6 at both the transcriptional and translational levels. Further investigations reveal that these effects mainly act via suppressing JNK-mediated AP-1 rather than the NF-κB pathway; these effects include a decrease in the phosphorylation level of JNK and a direct inhibition of the activity of p-JNK.
CONCLUSIONS:
These data provide scientific molecular evidence that Curcumol may be a potential lead compound for a novel anti-inflammatory drug because of its inhibitory activity on the production of various inflammatory mediators.

Curcumol from Rhizoma Curcumae suppresses epileptic seizure by facilitation of GABA(A) receptors.[Pubmed: 24565642 ]

Neuropharmacology. 2014 Jun;81:244-55.

Rhizoma Curcumae is a common Chinese dietary spice used in South Asia and China for thousands of years. As the main extract, Rhizoma Curcumae oil has attracted a great interest due to its newly raised therapeutic activities including its pharmacological effects upon central nervous system such as neuroprotection, cognitive enhancement, and anti-seizure efficacy; however the molecular mechanisms and the target identification remain to be established.
METHODS AND RESULTS:
Here we characterize an inhibitory effect of Curcumol, a major bioactive component of Rhizoma Curcumae oil, on the excitability of hippocampal neurons in culture, the basal locomotor activity of freely moving animals, and the chemically induced seizure activity in vivo. Electrophysiological recording showed that acute application of Curcumol significantly facilitated the γ-aminobutyric acid (GABA)-activated current in cultured mouse hippocampal neurons and in human embryonic kidney cells expressing α1- or α5-containing A type GABA (GABAA) receptors in a concentration-dependent manner. Measurement of tonic and miniature inhibitory postsynaptic GABAergic currents in hippocampal slices indicated that Curcumol enhanced both forms of inhibition. In both pentylenetetrazole and kainate seizure models, Curcumol suppressed epileptic activity in mice by prolonging the latency to clonic and tonic seizures and reducing the mortality as well as the susceptibility to seizure, presumably by facilitating the activation of GABAA receptors.
METHODS AND RESULTS:
Taken together, our results identified Curcumol as a novel anti-seizure agent which inhibited neuronal excitability through enhancing GABAergic inhibition.

In vivo

Curcumol Inhibits Growth and Induces Apoptosis of Colorectal Cancer LoVo Cell Line via IGF-1R and p38 MAPK Pathway[Pubmed: 26307972]

Int J Mol Sci. 2015 Aug; 16(8): 19851–67.

Curcumol, isolated from the traditional medical plant Rhizoma Curcumae, is the bioactive component of Zedoary oil, whose potential anti-tumor effect has attracted considerable attention in recent years. Though many researchers have reported Curcumol and its bioactivity, the potential molecular mechanism for its anti-cancer effect in colorectal cancer LoVo cells still remains unclear.
METHODS AND RESULTS:
In the present study, we found that Curcumol showed growth inhibition and induced apoptosis of LoVo cells in a dose- and time-dependent manner. The occurrence of its proliferation inhibition and apoptosis came with suppression of IGF-1R expression, and then increased the phosphorylation of p38 mitogen activated protein kinase (MAPK), which might result in a cascade response by inhibiting the CREB survival pathway and finally triggered Bax/Bcl-2 and poly(ADP-ribose) polymerase 1 (PARP-1) apoptosis signals. Moreover, Curcumol inhibited colorectal cancer in xenograft models of nude mice. Immunohistochemical and Western blot analysis revealed that Curcumol could decrease the expression of ki-67, Bcl-2 as well as CREB1, and increase the expression of Bax and the phosphorylation of p38, which were consistent with our in vitro study.
CONCLUSIONS:
Overall, our in vitro and in vivo data confirmed the anti-cancer activity of Curcumol, which was related to a significant inhibition of IGF-1R and activation of p38 MAPKs, indicating that Curcumol may be a potential anti-tumor agent for colorectal carcinoma therapy.

Protocol of Curcumol

Cell Research

Inhibitory Effect of Curcumol on Jak2-STAT Signal Pathway Molecules of Fibroblast-Like Synoviocytes in Patients with Rheumatoid Arthritis.[Pubmed: 22474524]

Curcumol suppresses RANKL-induced osteoclast formation by attenuating the JNK signaling pathway.[Pubmed: 24732351]

Biochem Biophys Res Commun. 2014 May 2;447(2):364-70.

Osteoclasts, derived from hemopoietic progenitors of the monocyte/macrophage lineage, have a unique role in bone resorption, and are considered a potential therapeutic target in the treatment of such pathologic bone diseases as osteoporosis, rheumatoid arthritis, and periodontitis.
METHODS AND RESULTS:
In the present study, we demonstrate that Curcumol, one of the major components of the essential oil of Rhizoma Curcumae, exhibits an inhibitory effect on receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclast differentiation with both bone marrow-derived macrophages and RAW264.7 cells in a dose-dependent manner. In addition, RANKL-induced mRNA expression of osteoclast-specific genes, such as tartrate-resistant acid phosphatase, calcitonin receptor, and cathepsin K, is prominently reduced in the presence of Curcumol. Furthermore, the molecular mechanism of action was investigated, and Curcumol inhibited osteoclastogenesis by specifically impairing RANKL-induced c-Jun N-terminal kinase (JNK)/activator protein-1 (AP-1) signaling, which was further identified in rescue studies by means of anisomycin, a JNK signaling-specific activator.
CONCLUSIONS:
Taken together, these findings suggest that Curcumol suppresses RANKL-induced osteoclast differentiation through the JNK/AP-1 signaling pathway, and may be useful as a therapeutic treatment for bone resorption-associated diseases.

Evid Based Complement Alternat Med. 2012;2012:746426.

Hyperplasia of synovial membrane in rheumatoid arthritis (RA) is a critical pathological foundation for inducing articular injury. The janus kinase and signal transducer and activator of transcription (Jak-STAT) pathway plays a critical role in synovial membrane proliferation induced by platelet-derived growth factor (PDGF). To explore the anti-cell proliferation mechanism of Curcumol, a pure monomer extracted from Chinese medical plant zedoary rhizome, the changes of Jak2-STAT1/3 signal pathway-related molecules in synoviocytes were observed in vitro.
METHODS AND RESULTS:
In this study, the fibroblast-like synoviocytes (FLS) in patients with RA were collected and cultured. The following parameters were measured: cell proliferation (WST-1 assay), cell cycles (fluorescence-activated cell sorting, FACS), STAT1 and STAT3 activities (electrophoretic mobility shift assay, EMSA), and the protein expressions of phosphorylated Jak2, STAT1, and STAT3 (Western blot). It was shown that Curcumol could inhibit the RA-FLS proliferation and DNA synthesis induced by PDGF-BB in a dose-dependent manner in vitro. The transcription factors activities of STAT1 and STAT3 were obviously elevated after PDGF-BB stimulation (P < 0.05). Super-shift experiments identified the STAT1 or STAT3 proteins in the complex. Furthermore, the different concentration Curcumol could downregulate the DNA binding activities of STAT1 and STAT3 (P < 0.05) and inhibit the phosphorylation of Jak2 while it had no effect on the protein expressions of STAT1 and STAT3. Positive correlations were found between changes of cell proliferation and DNA-binding activities of STAT1 and STAT3, respectively (P < 0.01).
CONCLUSIONS:
In conclusion, Curcumol might suppress the FLS proliferation and DNA synthesis induced by PDGF-BB through attenuating Jak2 phosphorylation, downregulating STAT1 and STAT3 DNA-binding activities, which could provide theoretical foundation for clinical treatment of RA.activities, which could provide theoretical foundation for clinical treatment of RA.

Curcumol Dilution Calculator

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Preparing Stock Solutions of Curcumol

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.231 mL 21.1551 mL 42.3101 mL 84.6203 mL 105.7753 mL
5 mM 0.8462 mL 4.231 mL 8.462 mL 16.9241 mL 21.1551 mL
10 mM 0.4231 mL 2.1155 mL 4.231 mL 8.462 mL 10.5775 mL
50 mM 0.0846 mL 0.4231 mL 0.8462 mL 1.6924 mL 2.1155 mL
100 mM 0.0423 mL 0.2116 mL 0.4231 mL 0.8462 mL 1.0578 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 Curcumol

Curcumol is a sesquiterpene originally isolated from curcuma rhizomes; shows anticancer activities both in vitro and in vivo. IC50 value: Target: Anticancer natural compound in vitro: Curcumol exhibited time- and concentration-dependent anti-proliferative effects in SPC-A-1 human lung adenocarcinoma cells with cell cycle arrest in the G0/G1 phase while apoptosis-induction was also confirmed with flow cytometry and morphological analyses [1]. Curcumol-induced growth inhibition correlated with apoptosis induction as evidenced by Annexin V staining, and cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP) in HSC-T6. Suppression of the NF-κB translocation via inhibition of IκB-α phosphorylation by the curcumol led to the inhibition of expression of NF-κB-regulated gene, e.g. Bcl-xL and Bcl-2, in a PI3K-dependent manner, which is upstream of NF-κB activation [2]. Curcumol exhibits an inhibitory effect on receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclast differentiation with both bone marrow-derived macrophages and RAW264.7 cells in a dose-dependent manner [3]. in vivo: Anti-neoplastic effects of curcumol were also confirmed in tumor bearing mice. Curcumol (60 mg/kg daily) significantly reduced tumor size without causing notable toxicity [1].

References:
[1]. Tang QL, et al. Curcumol induces apoptosis in SPC-A-1 human lung adenocarcinoma cells and displays anti-neoplastic effects in tumor bearing mice. Asian Pac J Cancer Prev. 2015;16(6):2307-12. [2]. Chen G, et al. Curcumol induces HSC-T6 cell death through suppression of Bcl-2: involvement of PI3K and NF-κB pathways. Eur J Pharm Sci. 2014 Dec 18;65:21-8. [3]. Yu M, et al. Curcumol suppresses RANKL-induced osteoclast formation by attenuating the JNK signaling pathway. Biochem Biophys Res Commun. 2014 May 2;447(2):364-70.

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References on Curcumol

Curcumol exhibits anti-inflammatory properties by interfering with the JNK-mediated AP-1 pathway in lipopolysaccharide-activated RAW264.7 cells.[Pubmed:24269960]

Eur J Pharmacol. 2014 Jan 15;723:339-45.

Curcumol is one of the major components of the essential oil of Rhizoma Curcumae, a common traditional Chinese medicine with anti-inflammatory properties. However, the anti-inflammatory activity and the underlying molecular mechanisms of this compound remain unclear. In the present study, the anti-inflammation effect of Curcumol on lipopolysaccharide (LPS)-induced RAW264.7 cells is demonstrated along with its underlying mechanisms. We show that Curcumol inhibits LPS-induced NO production by suppressing iNOS mRNA expression and protein level but not iNOS activity. Moreover, Curcumol inhibits LPS-induced production of TNF-alpha, IL-1beta and IL-6 at both the transcriptional and translational levels. Further investigations reveal that these effects mainly act via suppressing JNK-mediated AP-1 rather than the NF-kappaB pathway; these effects include a decrease in the phosphorylation level of JNK and a direct inhibition of the activity of p-JNK. These data provide scientific molecular evidence that Curcumol may be a potential lead compound for a novel anti-inflammatory drug because of its inhibitory activity on the production of various inflammatory mediators.

Inhibitory Effect of Curcumol on Jak2-STAT Signal Pathway Molecules of Fibroblast-Like Synoviocytes in Patients with Rheumatoid Arthritis.[Pubmed:22474524]

Evid Based Complement Alternat Med. 2012;2012:746426.

Hyperplasia of synovial membrane in rheumatoid arthritis (RA) is a critical pathological foundation for inducing articular injury. The janus kinase and signal transducer and activator of transcription (Jak-STAT) pathway plays a critical role in synovial membrane proliferation induced by platelet-derived growth factor (PDGF). To explore the anti-cell proliferation mechanism of Curcumol, a pure monomer extracted from Chinese medical plant zedoary rhizome, the changes of Jak2-STAT1/3 signal pathway-related molecules in synoviocytes were observed in vitro. In this study, the fibroblast-like synoviocytes (FLS) in patients with RA were collected and cultured. The following parameters were measured: cell proliferation (WST-1 assay), cell cycles (fluorescence-activated cell sorting, FACS), STAT1 and STAT3 activities (electrophoretic mobility shift assay, EMSA), and the protein expressions of phosphorylated Jak2, STAT1, and STAT3 (Western blot). It was shown that Curcumol could inhibit the RA-FLS proliferation and DNA synthesis induced by PDGF-BB in a dose-dependent manner in vitro. The transcription factors activities of STAT1 and STAT3 were obviously elevated after PDGF-BB stimulation (P < 0.05). Super-shift experiments identified the STAT1 or STAT3 proteins in the complex. Furthermore, the different concentration Curcumol could downregulate the DNA binding activities of STAT1 and STAT3 (P < 0.05) and inhibit the phosphorylation of Jak2 while it had no effect on the protein expressions of STAT1 and STAT3. Positive correlations were found between changes of cell proliferation and DNA-binding activities of STAT1 and STAT3, respectively (P < 0.01). In conclusion, Curcumol might suppress the FLS proliferation and DNA synthesis induced by PDGF-BB through attenuating Jak2 phosphorylation, downregulating STAT1 and STAT3 DNA-binding activities, which could provide theoretical foundation for clinical treatment of RA.

Curcumol from Rhizoma Curcumae suppresses epileptic seizure by facilitation of GABA(A) receptors.[Pubmed:24565642]

Neuropharmacology. 2014 Jun;81:244-55.

Rhizoma Curcumae is a common Chinese dietary spice used in South Asia and China for thousands of years. As the main extract, Rhizoma Curcumae oil has attracted a great interest due to its newly raised therapeutic activities including its pharmacological effects upon central nervous system such as neuroprotection, cognitive enhancement, and anti-seizure efficacy; however the molecular mechanisms and the target identification remain to be established. Here we characterize an inhibitory effect of Curcumol, a major bioactive component of Rhizoma Curcumae oil, on the excitability of hippocampal neurons in culture, the basal locomotor activity of freely moving animals, and the chemically induced seizure activity in vivo. Electrophysiological recording showed that acute application of Curcumol significantly facilitated the gamma-aminobutyric acid (GABA)-activated current in cultured mouse hippocampal neurons and in human embryonic kidney cells expressing alpha1- or alpha5-containing A type GABA (GABAA) receptors in a concentration-dependent manner. Measurement of tonic and miniature inhibitory postsynaptic GABAergic currents in hippocampal slices indicated that Curcumol enhanced both forms of inhibition. In both pentylenetetrazole and kainate seizure models, Curcumol suppressed epileptic activity in mice by prolonging the latency to clonic and tonic seizures and reducing the mortality as well as the susceptibility to seizure, presumably by facilitating the activation of GABAA receptors. Taken together, our results identified Curcumol as a novel anti-seizure agent which inhibited neuronal excitability through enhancing GABAergic inhibition.

Curcumol induces HSC-T6 cell death through suppression of Bcl-2: involvement of PI3K and NF-kappaB pathways.[Pubmed:25220584]

Eur J Pharm Sci. 2014 Dec 18;65:21-8.

The major feature in the molecular pathogenesis of hepatic fibrosis requires maintenance of the activated hepatic stellate cells (HSCs) phenotype by both proliferation and inhibition of apoptosis. Thus, the induction of activated HSCs apoptosis has been proposed as an antifibrotic treatment strategy. Curcumol has pro-apoptotic activity in a number of cancer cell types. The aim of this study is to test the hypothesis that the interruption of the phosphatidylinositol 3 kinase (PI3K)/nuclear factor-kappaB (NF-kappaB) signaling pathway by Curcumol might induce apoptosis of activated HSCs. Our results indicated that Curcumol-induced growth inhibition correlated with apoptosis induction as evidenced by Annexin V staining, and cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP) in HSC-T6. Importantly, we show that the apoptotic effect of Curcumol was specific to the activated HSCs (HSC-T6). Suppression of the NF-kappaB translocation via inhibition of IkappaB-alpha phosphorylation by the Curcumol led to the inhibition of expression of NF-kappaB-regulated gene, e.g. Bcl-xL and Bcl-2, in a PI3K-dependent manner, which is upstream of NF-kappaB activation. Also, Curcumol-mediated apoptosis of HSC-T6 were reversed by LY294002 and Bay 11-7082. Taken together, our findings perfectly support the hypothesis and demonstrate that the inhibition of PI3K/NF-kappaB pathway by Curcumol lead to HSC-T6 apoptosis. Thus, our study indicates that Curcumol is a potential candidate for further preclinical study aimed at the treatment of liver fibrosis.

Curcumol Inhibits Growth and Induces Apoptosis of Colorectal Cancer LoVo Cell Line via IGF-1R and p38 MAPK Pathway.[Pubmed:26307972]

Int J Mol Sci. 2015 Aug 20;16(8):19851-67.

Curcumol, isolated from the traditional medical plant Rhizoma Curcumae, is the bioactive component of Zedoary oil, whose potential anti-tumor effect has attracted considerable attention in recent years. Though many researchers have reported Curcumol and its bioactivity, the potential molecular mechanism for its anti-cancer effect in colorectal cancer LoVo cells still remains unclear. In the present study, we found that Curcumol showed growth inhibition and induced apoptosis of LoVo cells in a dose- and time-dependent manner. The occurrence of its proliferation inhibition and apoptosis came with suppression of IGF-1R expression, and then increased the phosphorylation of p38 mitogen activated protein kinase (MAPK), which might result in a cascade response by inhibiting the CREB survival pathway and finally triggered Bax/Bcl-2 and poly(ADP-ribose) polymerase 1 (PARP-1) apoptosis signals. Moreover, Curcumol inhibited colorectal cancer in xenograft models of nude mice. Immunohistochemical and Western blot analysis revealed that Curcumol could decrease the expression of ki-67, Bcl-2 as well as CREB1, and increase the expression of Bax and the phosphorylation of p38, which were consistent with our in vitro study. Overall, our in vitro and in vivo data confirmed the anti-cancer activity of Curcumol, which was related to a significant inhibition of IGF-1R and activation of p38 MAPKs, indicating that Curcumol may be a potential anti-tumor agent for colorectal carcinoma therapy.

Curcumol suppresses RANKL-induced osteoclast formation by attenuating the JNK signaling pathway.[Pubmed:24732351]

Biochem Biophys Res Commun. 2014 May 2;447(2):364-70.

Osteoclasts, derived from hemopoietic progenitors of the monocyte/macrophage lineage, have a unique role in bone resorption, and are considered a potential therapeutic target in the treatment of such pathologic bone diseases as osteoporosis, rheumatoid arthritis, and periodontitis. In the present study, we demonstrate that Curcumol, one of the major components of the essential oil of Rhizoma Curcumae, exhibits an inhibitory effect on receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclast differentiation with both bone marrow-derived macrophages and RAW264.7 cells in a dose-dependent manner. In addition, RANKL-induced mRNA expression of osteoclast-specific genes, such as tartrate-resistant acid phosphatase, calcitonin receptor, and cathepsin K, is prominently reduced in the presence of Curcumol. Furthermore, the molecular mechanism of action was investigated, and Curcumol inhibited osteoclastogenesis by specifically impairing RANKL-induced c-Jun N-terminal kinase (JNK)/activator protein-1 (AP-1) signaling, which was further identified in rescue studies by means of anisomycin, a JNK signaling-specific activator. Taken together, these findings suggest that Curcumol suppresses RANKL-induced osteoclast differentiation through the JNK/AP-1 signaling pathway, and may be useful as a therapeutic treatment for bone resorption-associated diseases.

Description

Curcumol is a sesquiterpene originally isolated from curcuma rhizomes; shows anticancer activities both in vitro and in vivo.

Keywords:

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