|Source:||The rhizomes of Curcuma longa L.|
|Biological Activity or Inhibitors:||1. Curcumol has antitumor activity.
2. Curcumol induces HSC-T6 cell death through suppression of Bcl-2: involvement of PI3K and NF-κB pathways.
3. Curcumol suppresses RANKL-induced osteoclast formation by attenuating the JNK signaling pathway.
4. Curcumol has anti-inflammatory property, inhibit Jak2-STAT Signal Pathway Molecules of Fibroblast-Like Synoviocytes in Patients with Rheumatoid Arthritis.
5. Curcumol is a novel anti-seizure agent which inhibited neuronal excitability through enhancing GABAergic inhibition, it has inhibitory effects on the excitability of hippocampal neurons in culture, the basal locomotor activity of freely moving animals, and the chemically induced seizure activity in vivo.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|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|
Eur J Pharm Sci. 2014 Dec 18;65:21-8.
|Curcumol induces HSC-T6 cell death through suppression of Bcl-2: involvement of PI3K and NF-κB pathways.[Pubmed: 25220584]|
|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. Thus, our study indicates that Curcumol is a potential candidate for further preclinical study aimed at the treatment of liver fibrosis.|
Biochem Biophys Res Commun. 2014 May 2;447(2):364-70.
|Curcumol suppresses RANKL-induced osteoclast formation by attenuating the JNK signaling pathway.[Pubmed: 24732351]|
|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.|
Eur J Pharmacol. 2014 Jan 15;723:339-45.
|Curcumol exhibits anti-inflammatory properties by interfering with the JNK-mediated AP-1 pathway in lipopolysaccharide-activated RAW264.7 cells.[Pubmed: 24269960]|
|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. 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.|
Evid Based Complement Alternat Med. 2012;2012:746426.
|Inhibitory Effect of Curcumol on Jak2-STAT Signal Pathway Molecules of Fibroblast-Like Synoviocytes in Patients with Rheumatoid Arthritis.[Pubmed: 22474524]|
|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.|
Neuropharmacology. 2014 Jun;81:244-55.
|Curcumol from Rhizoma Curcumae suppresses epileptic seizure by facilitation of GABA(A) receptors.[Pubmed: 24565642 ]|
|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. Taken together, our results identified Curcumol as a novel anti-seizure agent which inhibited neuronal excitability through enhancing GABAergic inhibition.|
Int J Mol Sci. 2015 Aug; 16(8): 19851–67.
|Curcumol Inhibits Growth and Induces Apoptosis of Colorectal Cancer LoVo Cell Line via IGF-1R and p38 MAPK Pathway[Pubmed: 26307972]|
|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.|