|Description:||1. 6-Gingerol has been known to possess anti-tumorigenic and pro-apoptotic activities, it stimulates apoptosis through upregulation of NAG-1 and G1 cell cycle arrest through downregulation of cyclin D1, multiple mechanisms appear to be involved in 6-gingerol action, including protein degradation as well as β-catenin, PKCε, and GSK-3β pathways. |
2. 6-Gingerol and 6-shogaol may both exert anti-invasive activity against hepatoma cells through regulation of MMP-9 and TIMP-1, inhibition of the MAPK and PI3k/Akt pathways and NF-κB and STAT3 activities to suppress expression of MMP-2/-9 and uPA and block angiogenesis, and that 6-shogaol could further regulate urokinase-type plasminogen activity.
3. 6-Gingerol can repress quorum sensing (QS)-induced genes, specifically those related to the production of virulence factors, inducing exoprotease, rhamnolipid, and pyocyanin.
4. 6-Gingerol has antioxidant and anti-inflammatory activities, it induces genotoxicity probably by oxidative stress; lysosomal and mitochondrial damage were observed in 6-gingerol-induced toxicity.
5. 6-Gingerol has anti-adipogenic activity , can effectively suppress adipogenesis and that it exerts its role mainly through the significant down-regulation of PPARγ and C/EBPα and subsequently inhibits FAS and aP2 expression, also inhibit differentiation in 3T3-L1 cells by attenuating the Akt/GSK3β pathway.
|Targets:||Wnt/β-catenin | PKC | GSK-3 | MMP(e.g.TIMP) | MAPK | PI3K | NF-kB | STAT | PPAR | ROS | Akt|
|Source:||The rhizomes of Zingber officinale Rosc.|
|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||3.3967 mL||16.9837 mL||33.9674 mL||67.9348 mL||84.9185 mL|
|5 mM||0.6793 mL||3.3967 mL||6.7935 mL||13.587 mL||16.9837 mL|
|10 mM||0.3397 mL||1.6984 mL||3.3967 mL||6.7935 mL||8.4918 mL|
|50 mM||0.0679 mL||0.3397 mL||0.6793 mL||1.3587 mL||1.6984 mL|
|100 mM||0.034 mL||0.1698 mL||0.3397 mL||0.6793 mL||0.8492 mL|
Sci Rep. 2015 Mar 2;5:8656.
|6-Gingerol reduces Pseudomonas aeruginosa biofilm formation and virulence via quorum sensing inhibition.[Pubmed: 25728862]|
|Pseudomonas aeruginosa is a well-known pathogenic bacterium that forms biofilms and produces virulence factors via quorum sensing (QS). Interfering with normal QS interactions between signal molecules and their cognate receptors is a developing strategy for attenuating its virulence. Here we tested the hypothesis that 6-Gingerol, a pungent oil of fresh ginger, reduces biofilm formation and virulence by antagonistically binding to P. aeruginosa QS receptors. In silico studies demonstrated molecular binding occurs between 6-Gingerol and the QS receptor LasR through hydrogen bonding and hydrophobic interactions. Experimentally 6-Gingerol reduced biofilm formation, several virulence factors (e.g., exoprotease, rhamnolipid, and pyocyanin), and mice mortality. Further transcriptome analyses demonstrated that 6-Gingerol successfully repressed QS-induced genes, specifically those related to the production of virulence factors. These results strongly support our hypothesis and offer insight into the molecular mechanism that caused QS gene repression.|
Phytomedicine. 2013 Apr 15;20(6):481-7.
|6-gingerol prevents adipogenesis and the accumulation of cytoplasmic lipid droplets in 3T3-L1 cells.[Pubmed: 23369342 ]|
|6-Gingerol ((S)-5-hydroxy-1-(4-hydroxy-3-methoxyphenyl)-3-decanone) is one of the pungent constituents of Zingiber zerumbet (L) Smith (Zingiberaceae family). In this study, we investigated the effects of 6-Gingerol on the inhibition of adipogenesis in 3T3-L1 cells. After treatment with 6-Gingerol in differentiation medium for 4 or 8 days, the 3T3-L1 cells were lysed for experimental analysis. Cells were stained with Oil-Red-O to detect oil droplets in adipocytes. The 3T3-L1 cells were lysed and measured for triglyceride contents. The protein expression of adipogenesis-related transcription factor was evaluated by Western blot analysis. 6-Gingerol suppressed oil droplet accumulation and reduced the droplet size in a concentration (5-15 μg/ml)- and time-dependent manner. Treatment of 3T3-L1 cells with 6-Gingerol reduced the protein levels of peroxisome proliferator-activated receptor (PPAR)γ and CCAAT/enhancer-binding protein (C/EBP)α. Additionally, the protein levels of fatty acid synthase (FAS) and adipocyte-specific fatty acid binding protein (aP2) decreased upon treatment with 6-Gingerol. Meanwhile, 6-Gingerol diminished the insulin-stimulated serine phosphorylation of Akt (Ser473) and GSK3β (Ser9). These results suggest that 6-Gingerol effectively suppresses adipogenesis and that it exerts its role mainly through the significant down-regulation of PPARγ and C/EBPα and subsequently inhibits FAS and aP2 expression. 6-Gingerol also inhibited differentiation in 3T3-L1 cells by attenuating the Akt/GSK3β pathway. Our findings provide important insights into the mechanisms underlying the anti-adipogenic activity of 6-Gingerol.|
Mol Nutr Food Res. 2012 Aug;56(8):1304-14.
|Molecular mechanism inhibiting human hepatocarcinoma cell invasion by 6-shogaol and 6-gingerol.[Pubmed: 22714996]|
|By gelatin zymography and luciferase reporter gene assays, we found that 6-Gingerol and 6-shogaol regulate MMP-2/-9 transcription. Moreover, 6-Gingerol directly decreased expression of uPA, but the 6-shogaol-mediated decrease in uPA was accompanied by up-regulation of plasminogen activator inhibitor (PAI)-1. 6-Gingerol and 6-shogaol concentrations of ≥ 10 μM and ≥ 2.5 μM, respectively, significantly inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) and PI3K/Akt signaling, the activation of NF-κB, and the translocation of NF-κB and STAT3. Incubation of 6-Gingerol or 6-shogaol with human umbilical vein endothelial cells or rat aortas significantly attenuated tube formation. CONCLUSION: 6-Shogaol and 6-Gingerol effectively inhibit invasion and metastasis of hepatocellular carcinoma through diverse molecular mechanisms, including inhibition of the MAPK and PI3k/Akt pathways and NF-κB and STAT3 activities to suppress expression of MMP-2/-9 and uPA and block angiogenesis.|
Mol Nutr Food Res. 2010 Nov;54(11):1618-27.
|Anti-invasion effects of 6-shogaol and 6-gingerol, two active components in ginger, on human hepatocarcinoma cells.[Pubmed: 20521273]|
|The migratory and invasive abilities of phorbol 12-myristate 13-acetate (PMA)-treated HepG2 and PMA-untreated Hep3B cells were both reduced in a dose-dependent manner by treatment with 6-shogaol and 6-Gingerol. Upon incubation of PMA-treated HepG2 cells and PMA-untreated Hep3B cells with 6-shogaol and 6-Gingerol, matrix metalloproteinase (MMP)-9 activity decreased, whereas the expression of tissue inhibitor metalloproteinase protein (TIMP)-1 increased in both cell types. Additionally, urokinase-type plasminogen activator activity was dose-dependently decreased in Hep3B cells after incubation with 6-shogaol for 24 h. Analysis with semi-quantitative reverse transcription-PCR showed that the regulation of MMP-9 by 6-shogaol and 6-Gingerol and the regulation of TIMP-1 by 6-shogaol in Hep3B cells may on the transcriptional level. CONCLUSIONS: These results suggest that 6-shogaol and 6-Gingerol might both exert anti-invasive activity against hepatoma cells through regulation of MMP-9 and TIMP-1 and that 6-shogaol could further regulate urokinase-type plasminogen activity.|
Chem Biol Interact. 2010 Apr 15;185(1):12-7.
|Genotoxic effect of 6-gingerol on human hepatoma G2 cells.[Pubmed: 20167213 ]|
|6-Gingerol, a major component of ginger, has antioxidant, anti-apoptotic, and anti-inflammatory activities. However, some dietary phytochemicals possess pro-oxidant effects as well, and the risk of adverse effects is increased by raising the use of doses. The aim of this study was to assess the genotoxic effects of 6-Gingerol and to clarify the mechanisms, using human hepatoma G2 (HepG2) cells. Exposure of the cells to 6-Gingerol caused significant increase of DNA migration in comet assay, increase of micronuclei frequencies at high concentrations at 20-80 and 20-40 microM, respectively. These results indicate that 6-Gingerol caused DNA strand breaks and chromosome damage. To further elucidate the underlying mechanisms, we tested lysosomal membrane stability, mitochondrial membrane potential, the intracellular generation of reactive oxygen species (ROS) and reduced glutathione (GSH). In addition, the level of oxidative DNA damage was evaluated by immunocytochemical analysis on 8-hydroxydeoxyguanosine (8-OHdG). Results showed that lysosomal membrane stability was reduced after treatment by 6-Gingerol (20-80 microM) for 40 min, mitochondrial membrane potential decreased after treatment for 50 min, GSH and ROS levels were significantly increased after treatment for 60 min. These suggest 6-Gingerol induces genotoxicity probably by oxidative stress; lysosomal and mitochondrial damage were observed in 6-Gingerol-induced toxicity.|
Mol Carcinog. 2008 Mar;47(3):197-208.
|Multiple mechanisms are involved in 6-gingerol-induced cell growth arrest and apoptosis in human colorectal cancer cells.[Pubmed: 18058799]|
|6-Gingerol, a natural product of ginger, has been known to possess anti-tumorigenic and pro-apoptotic activities. However, the mechanisms by which it prevents cancer are not well understood in human colorectal cancer. Cyclin D1 is a proto-oncogene that is overexpressed in many cancers and plays a role in cell proliferation through activation by beta-catenin signaling. Nonsteroidal anti-inflammatory drug (NSAID)-activated gene-1 (NAG-1) is a cytokine associated with pro-apoptotic and anti-tumorigenic properties. In the present study, we examined whether 6-Gingerol influences cyclin D1 and NAG-1 expression and determined the mechanisms by which 6-Gingerol affects the growth of human colorectal cancer cells in vitro. 6-Gingerol treatment suppressed cell proliferation and induced apoptosis and G(1) cell cycle arrest. Subsequently, 6-Gingerol suppressed cyclin D1 expression and induced NAG-1 expression. Cyclin D1 suppression was related to inhibition of beta-catenin translocation and cyclin D1 proteolysis. Furthermore, experiments using inhibitors and siRNA transfection confirm the involvement of the PKCepsilon and glycogen synthase kinase (GSK)-3beta pathways in 6-Gingerol-induced NAG-1 expression. The results suggest that 6-Gingerol stimulates apoptosis through upregulation of NAG-1 and G(1) cell cycle arrest through downregulation of cyclin D1. Multiple mechanisms appear to be involved in 6-Gingerol action, including protein degradation as well as beta-catenin, PKCepsilon, and GSK-3beta pathways.|