6-Gingerol CAS NO.23513-14-6

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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.

Chemical Properties of 6-Gingerol

Cas No.	23513-14-6
PubChem ID	442793	Appearance	Yellow oil
Formula	C17H26O4	M.Wt	294.4
Type of Compound	Phenols	Storage	Desiccate at -20°C
Synonyms	(S)-(+)-[6]Gingerol; 6-Gingerol
Solubility	DMSO : ≥ 50 mg/mL (169.84 mM) *"≥" means soluble, but saturation unknown.
Chemical Name	(5S)-5-hydroxy-1-(4-hydroxy-3-methoxyphenyl)decan-3-one
SMILES	CCCCCC(CC(=O)CCC1=CC(=C(C=C1)O)OC)O
Standard InChIKey	NLDDIKRKFXEWBK-AWEZNQCLSA-N
Standard InChI	InChI=1S/C17H26O4/c1-3-4-5-6-14(18)12-15(19)9-7-13-8-10-16(20)17(11-13)21-2/h8,10-11,14,18,20H,3-7,9,12H2,1-2H3/t14-/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 6-Gingerol

The rhizomes of Zingber officinale Rosc.

Biological Activity of 6-Gingerol

Description	6-Gingerol possesses anti-adipogenic, anti-tumorigenic, anti-invasive, antioxidant, anti-inflammatory, 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. 6-Gingerol 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
In vitro	6-gingerol prevents adipogenesis and the accumulation of cytoplasmic lipid droplets in 3T3-L1 cells.[Pubmed: 23369342 ] Phytomedicine. 2013 Apr 15;20(6):481-7. 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). METHODS AND RESULTS: 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). CONCLUSIONS: 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. Anti-invasion effects of 6-shogaol and 6-gingerol, two active components in ginger, on human hepatocarcinoma cells.[Pubmed: 20521273] Mol Nutr Food Res. 2010 Nov;54(11):1618-27. Hepatocellular carcinoma is the most common type of liver cancer and is highly metastatic. Metastasis is considered to be the major cause of death in cancer patients. Ginger is a natural dietary rhizome with anti-oxidative, anti-inflammatory, and anti-carcinogenic activities. The aims of this study were to evaluate the anti-invasion activity of 6-shogaol and 6-Gingerol, two compounds found in ginger, on hepatoma cells. METHODS AND RESULTS: 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. Genotoxic effect of 6-gingerol on human hepatoma G2 cells.[Pubmed: 20167213 ] Chem Biol Interact. 2010 Apr 15;185(1):12-7. 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. METHODS AND RESULTS: 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. CONCLUSIONS: These suggest 6-Gingerol induces genotoxicity probably by oxidative stress; lysosomal and mitochondrial damage were observed in 6-Gingerol-induced toxicity.

Protocol of 6-Gingerol

Kinase Assay

Multiple mechanisms are involved in 6-gingerol-induced cell growth arrest and apoptosis in human colorectal cancer cells.[Pubmed: 18058799] Molecular mechanism inhibiting human hepatocarcinoma cell invasion by 6-shogaol and 6-gingerol.[Pubmed: 22714996] 6-Gingerol reduces Pseudomonas aeruginosa biofilm formation and virulence via quorum sensing inhibition.[Pubmed: 25728862] Sci Rep. 2015 Mar 2;5:8656. 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. METHODS AND RESULTS: 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. CONCLUSIONS: These results strongly support our hypothesis and offer insight into the molecular mechanism that caused QS gene repression. Mol Nutr Food Res. 2012 Aug;56(8):1304-14. We previously demonstrated that 6-shogaol and 6-Gingerol, two active compounds in ginger (Zingiber officinale), possess antiinvasive activity against highly metastatic hepatoma cells. The aims of this study were to evaluate the inhibitory effect and molecular mechanism underlying the transcription and translation of matrix metalloproteinases (MMPs) and urokinase-type plasminogen activator (uPA) in Hep3B cells as well as the antiangiogenic activity of 6-Gingerol and 6-shogaol. METHODS AND RESULTS: 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. CONCLUSIONS: 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 Carcinog. 2008 Mar;47(3):197-208. 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. METHODS AND RESULTS: 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. CONCLUSIONS: 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.

Preparing Stock Solutions of 6-Gingerol

	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
* 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.

 

References on 6-Gingerol

Genotoxic effect of 6-gingerol on human hepatoma G2 cells.[Pubmed:20167213]

Chem Biol Interact. 2010 Apr 15;185(1):12-7.

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.

Molecular mechanism inhibiting human hepatocarcinoma cell invasion by 6-shogaol and 6-gingerol.[Pubmed:22714996]

Mol Nutr Food Res. 2012 Aug;56(8):1304-14.

SCOPE: We previously demonstrated that 6-shogaol and 6-Gingerol, two active compounds in ginger (Zingiber officinale), possess antiinvasive activity against highly metastatic hepatoma cells. The aims of this study were to evaluate the inhibitory effect and molecular mechanism underlying the transcription and translation of matrix metalloproteinases (MMPs) and urokinase-type plasminogen activator (uPA) in Hep3B cells as well as the antiangiogenic activity of 6-Gingerol and 6-shogaol. METHODS AND RESULTS: 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 muM and >/= 2.5 muM, respectively, significantly inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) and PI3K/Akt signaling, the activation of NF-kappaB, and the translocation of NF-kappaB 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-kappaB and STAT3 activities to suppress expression of MMP-2/-9 and uPA and block angiogenesis.

Multiple mechanisms are involved in 6-gingerol-induced cell growth arrest and apoptosis in human colorectal cancer cells.[Pubmed:18058799]

Mol Carcinog. 2008 Mar;47(3):197-208.

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.

6-gingerol prevents adipogenesis and the accumulation of cytoplasmic lipid droplets in 3T3-L1 cells.[Pubmed:23369342]

Phytomedicine. 2013 Apr 15;20(6):481-7.

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 mug/ml)- and time-dependent manner. Treatment of 3T3-L1 cells with 6-Gingerol reduced the protein levels of peroxisome proliferator-activated receptor (PPAR)gamma and CCAAT/enhancer-binding protein (C/EBP)alpha. 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 GSK3beta (Ser9). These results suggest that 6-Gingerol effectively suppresses adipogenesis and that it exerts its role mainly through the significant down-regulation of PPARgamma and C/EBPalpha and subsequently inhibits FAS and aP2 expression. 6-Gingerol also inhibited differentiation in 3T3-L1 cells by attenuating the Akt/GSK3beta pathway. Our findings provide important insights into the mechanisms underlying the anti-adipogenic activity of 6-Gingerol.

Anti-invasion effects of 6-shogaol and 6-gingerol, two active components in ginger, on human hepatocarcinoma cells.[Pubmed:20521273]

Mol Nutr Food Res. 2010 Nov;54(11):1618-27.

SCOPE: Hepatocellular carcinoma is the most common type of liver cancer and is highly metastatic. Metastasis is considered to be the major cause of death in cancer patients. Ginger is a natural dietary rhizome with anti-oxidative, anti-inflammatory, and anti-carcinogenic activities. The aims of this study were to evaluate the anti-invasion activity of 6-shogaol and 6-Gingerol, two compounds found in ginger, on hepatoma cells. METHODS AND RESULTS: 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.

6-Gingerol reduces Pseudomonas aeruginosa biofilm formation and virulence via quorum sensing inhibition.[Pubmed:25728862]

Sci Rep. 2015 Mar 2;5:8656.

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.

Description

[6]-Gingerol is an active compound isolated from Ginger (Zingiber officinale Rosc), exhibits a variety of biological activities including anticancer, anti-inflammation, and anti-oxidation.

Keywords:

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