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  • Brand : BIOFRON

  • Catalogue Number : BD-P0784

  • Specification : 98.5%(HPLC)

  • CAS number : 555-66-8

  • Volume : 500mg

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Catalogue Number


Analysis Method






Molecular Weight


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Structure Type





(E)-1-(4-Hydroxy-3-methoxy-phenyl)-dec-4-en-3-one/(4E)-1-(4-Hydroxy-3-methoxyphenyl)dec-4-en-3-one/6-Shogaol/Trans-6-Shogaol/4-Decen-3-one, 1-(4-hydroxy-3-methoxyphenyl)/Shogaol/4-Decen-3-one, 1-(4-hydroxy-3-methoxyphenyl)-, (4E)-/(4E)-1-(4-Hydroxy-3-methoxyphenyl)-4-decen-3-one/[6]-Shogaol



Bioactive Constituent of Ginger, 6-Shogaol, Prevents Adipogenesis and Stimulates Lipolysis in 3T3-L1 Adipocytes (vol 40, pg 84, 2016) PUMID/DOI:DOI: 10.1111/jfbc.12277 Suk S, Seo S G, Yu J G, et al. Erratum[J]. Journal of Food Biochemistry, 2016, 40(2):84–90. Zingiber officinale Roscoe, one of the most widely used spices, has been reported to have anti-obesity and anti-diabetes effects. In the present study, we investigated the effects of 6-shogaol, a bioactive compound present in ginger, on the adipogenic process in 3T3-L1 preadipocytes. The anti-adipogenic effects of 6-shogaol was significantly higher than the more widely investigated 6-gingerol, another major ginger constituent. We observed that 6-shogaol inhibited the expression of two master regulators of adipogenesis, PPARγ and C/EBPα, and also stimulated lipolysis in mature 3T3-L1 adipocytes. Collectively, these results suggest that 6-shogaol, not 6-gingerol, is the major compound present in ginger responsible for its reported anti-adipogenic properties.Practical ApplicationsGinger is widely consumed all over the world, and has been associated with various health benefits. At least some of these benefits have been previously attributed to 6-gingerol. In the present study, we observed that 6-shogaol has more potent anti-adipogenic effects than 6-gingerol in 3T3-L1 cells. This is the first study to investigate the anti-obesity effect of 6-shogaol in vitro, and provides a new perspective on future development of ginger-based anti-obesity str ategies. 6-Shogaol Protects against Oxidized LDL-Induced Endothelial Injruries by Inhibiting Oxidized LDL-Evoked LOX-1 Signaling. PUMID/DOI:DOI:10.1155/2013/503521 Endothelial dysfunction and oxLDL are believed to be early and critical events in atherogenesis. 6-Shogaol is the major bioactive compound present in Zingiber officinale and possesses the anti-atherosclerotic effect. However, the mechanisms remain poorly understood. The goal of this study was to investigate the effects of 6-shogaol on oxLDL-induced Human umbilical vein endothelial cells (HUVECs) injuries and its possible molecular mechanisms. Hence, we studied the effects of 6-shogaol on cell apoptosis, cellular reactive oxygen species (ROS), NF- kappa B activation, Bcl-2 expression, and caspase -3, -8, -9 activities. In addition, E-selectin, MCP-1, and ICAM-1 were determined by ELISA. Our study show that oxLDL increased LOX-1 expression, ROS levels, NF- kappa B, caspases-9 and -3 activation and decreased Bcl-2 expression in HUVECs. These alterations were attenuated by 6-shogaol. Cotreatment with 6-shogaol and siRNA of LOX-1 synergistically reduced oxLDL-induced caspases -9, -3 activities and cell apoptosis. Overexpression of LOX-1 attenuated the protection by 6-shogaol and suppressed the effects of 6-shogaol on oxLDL-induced oxidative stress. In addition, oxLDL enhanced the activation of NF- kappa B and expression of adhesion molecules. Pretreatment with 6-shogaol, however, exerted significant cytoprotective effects in all events. Our data indicate that 6-shogaol might be a potential natural antiapoptotic agent for the treatment of atherosclerosis. Pharmacological studies on ginger. IV. Effect of (6)-shogaol on the arachidonic cascade PUMID/DOI:Suekawa M, Yuasa K, Isono M, et al. [Pharmacological studies on ginger. IV. Effect of (6)-shogaol on the arachidonic cascade][J]. Nihon Yakurigaku Zasshi Folia Pharmacologica Japonica, 1986, 88(4):263. (6)-Shogaol, a pungent component of ginger, which is contained in semi-dried ginger but is rarely found in fresh ginger inhibited carrageenin-induced swelling of hind paw in rats and arachidonic acid (AA)-induced platelet aggregation in rabbits. Moreover, (6)-shogaol prevented prostaglandin I2 (PGI2) release from the aorta of rats when tested as an inhibitor of platelet aggregation. These results suggest that (6)-shogaol may have an inhibitory action on the cyclo-oxygenases in both platelets and aorta. Examination of the effects of (6)-shogaol on cyclo-oxygenases in rabbit platelets and microsome fractions of rat aorta indicated that (6)-shogaol inhibited cyclo-oxygenase activities of both tissues in a concentration-dependent manner. Furthermore, when we examined the effect of (6)-shogaol on 5-lipoxygenase from RBL-1 cells, (6)-shogaol exhibited an inhibitory action on 5-lipoxygenase activity. Therefore, it seems that the inhibitory effects of (6)-shogaol on the carrageenin-induced paw edema, AA-induced platelet aggregation and PGI2 production of aorta may be caused by the inhibition of cyclo-oxygenase activity. Cytoprotective and Anti-inflammatory Effects of 6-Shogaol on Human Dermal Fibroblasts PUMID/DOI:DOI: 10.20402/ajbc.2016.0158 Lee N K, Ku J E, Han H S. Cytoprotective and Anti-inflammatory Effects of 6-Shogaol on Human Dermal Fibroblasts[J]. 2017, 15(3):367-376. Purpose: 6-Shogaol is one of the spicy flavor ingredients of ginger and hydrolysis product of gingerols. The purpose of this study is to investigate the potential of 6-shogaol as a natural cosmetic raw material by examining cell protection and inflammation inhibitory activity in human dermal fibroblasts (HDFs). Methods: To verify the cytoprotective effects of 6-shogaol, cell viability was measured by watersoluble tetrazolium salt (WST-1) assay. To verify the anti-inflammatory effects of 6-shogaol, we performed nuclear factor kappa-light-chain-enhancer of activated B cells (NFΚB) promoter luciferase assay to check the expression of NFΚB. Additionally, the expression of inflmmation related gene such as cyclooxygenase 2 (COX2), receptor for advanced glycation end product (RAGE), tumor necrosis factor alpha (TNFΑ), interleukin 6 (IL6), and interleukin 8 (IL8) mRNA was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Results: 6-Shogaol showed no toxicity in HDFs at concentrations of 5, 10, 20, and 40 μM, respectively and the cell viability was increased in a dose dependent manner. qRT-PCR analysis showed 6-shogaol treatment downregulated the expression of NFΚB, COX2, RAGE, TNFΑ , IL6, and IL8 in a dose dependent manner, resulting that 6-shogaol leads to protective activities against inflammatory responses in HDFs. Conclusion: As mentioned above, 6-shogaol restored cell viability and decreased the expression of inflammatory factors in a dose dependent manner. Consequently, these results suggest the possibility of 6-shogaol as cosmetic material preventing skin aging, through identifid functions on cytoprotection and anti-inflmmation. 6-Shogaol attenuates LPS-induced inflammation in BV2 microglia cells by activating PPAR-gamma PUMID/DOI:DOI: 10.18632/oncotarget.16719 Oncotarget. 2017 Jun 27;8(26):42001-42006. 6-Shogaol, a pungent agent isolated from Zingiber officinale Roscoe, has been known to have anti-tumor and anti-inflammatory effects. However, the anti-inflammatory effects and biological mechanism of 6-Shogaol in LPS-activated BV2 microglia remains largely unknown. In this study, we evaluated the anti-inflammatory effects of 6-Shogaol in LPS-activated BV2 microglia. 6-Shogaol was administrated 1 h before LPS treatment. The production of inflammatory mediators were detected by ELISA. The expression of NF-kappa B and PPAR-gamma were detected by western blot analysis. Our results revealed that 6-Shogaol inhibited LPS-induced TNF-alpha, IL-1 beta, IL-6, and PGE2 production in a concentration dependent manner. Furthermore, 6-Shogaol inhibited LPS-induced NF-kappa B activation by inhibiting phosphorylation and nuclear translocation of NF-kappa B p65. In addition, 6-Shogaol could increase the expression of PPAR-gamma. Moreover, inhibition of PPAR-gamma by GW9662 could prevent the inhibition of 6-Shogaol on LPS-induced inflammatory mediator production. In conclusion, 6-Shogaol inhibits LPS-induced inflammation by activating PPAR-gamma. Protection by [6]-shogaol against lipopolysaccharide-induced toxicity in murine astrocytes is related to production of brain-derived neurotrophic factor PUMID/DOI:DOI: 10.1016/j.fct.2011.11.042 Food Chem Toxicol. 2012 Mar;50(3-4):597-602. [6]-Shogaol has beneficial effects in spinal neuronal regeneration, but associated molecules and mechanisms are not identified. Neurotrophic factors, including brain-derived neurotrophic factor (BDNF), are associated with proliferation and differentiation of neuronal cells and exert a neuroprotective effect in neurodegenerative models. We investigated whether treatment with [6]-shogaol increases BDNF expression in lipopolysaccharide (LPS)-treated astrocytes, and examined the effect of [6]-shogaol on neuronal protection. [6]-Shogaol significantly attenuated the cell death induced by LPS. Western blotting showed that [6]-shogaol treatment reduced Bax expression and increased B-cell lymphoma (Bcl)-2 and BclxL expression in LPS-treated cells, consistent with the effects of BDNF treatment. Furthermore, K252a, a blocker of neurotrophic factors, attenuated the cellular protective effects of [6]-shogaol and BDNF. This study provides the first evidence that [6]-shogaol increases the expression of BDNF in LPS-treated astrocytes. Furthermore, these experimental results indicate that production of BDNF in astrocytes might be related to altered cell viability following [6]-shogaol treatment. Thus, the neuroprotective effects of [6]-shogaol is mediated by up-regulation of BDNF. (C) 2011 Elsevier Ltd. All rights reserved. [6]-Shogaol inhibits alpha-MSH-induced melanogenesis through the acceleration of ERK and PI3K/Akt-mediated MITF degradation. PUMID/DOI:DOI:10.1155/2014/842569 Biomed Res Int. 2014;2014:842569. [6]-Shogaol is the main biologically active component of ginger. Previous reports showed that [6]-shogaol has several pharmacological characteristics, such as antioxidative, anti-inflammatory, antimicrobial, and anticarcinogenic properties. However, the effects of [6]-shogaol on melanogenesis remain to be elucidated. The study aimed to evaluate the potential skin whitening mechanisms of [6]-shogaol. The effects of [6]-shogaol on cell viability, melanin content, tyrosinase activity, and the expression of the tyrosinase and microphthalmia-associated transcription factor (MITF) were measured. The results revealed that [6]-shogaol effectively suppresses tyrosinase activity and the amount of melanin and that those effects are more pronounced than those of arbutin. It was also found that [6]-shogaol decreased the protein expression levels of tyrosinase-related protein 1 (TRP-1) and microphthalmia-associated transcriptional factor (MITF). In addition, the MITF mRNA levels were also effectively decreased in the presence of 20 muM [6]-shogaol. The degradation of MITF protein was inhibited by the MEK 1-inhibitor (U0126) or phosphatidylinositol-3-kinase inhibitor (PI3K inhibitor) (LY294002). Further immunofluorescence staining assay implied the involvement of the proteasome in the downregulation of MITF by [6]-shogaol. Our confocal assay results also confirmed that [6]-shogaol inhibited alpha-melanocyte stimulating hormone- (alpha-MSH-) induced melanogenesis through the acceleration of extracellular responsive kinase (ERK) and phosphatidylinositol-3-kinase- (PI3K/Akt-) mediated MITF degradation. 6-Shogaol, an Active Constituent of Dietary Ginger, Induces Autophagy by Inhibiting the AKT/mTOR Pathway in Human Non-Small Cell Lung Cancer A549 Cells PUMID/DOI:DOI: 10.1021/jf902315e J Agric Food Chem. 2009 Oct 28;57(20):9809-16. This study is the first study to investigate the anticancer effect of 6-shogaol in human non-small cell lung cancer A549 cells. 6-Shogaol inhibited cell proliferation by inducing autophagic cell death, but not, predominantly, apoptosis. Pretreatment of cells with 3-methyladenine (3-MA), an autophagy inhibitor, suppressed 6-shogaol mediated antiproliferation activity, suggesting that induction of autophagy by 6-shogaol is conducive to cell death. We also found that 6-shogaol inhibited survival signaling through the AKT/mTOR signaling pathway by blocking the activation of AKT and downstream targets, including the mammalian target of rapamycin (mTOR), forkhead transcription factors (FKHR) and glycogen synthase kinase-3 beta (GSK-3 beta). Phosphorylation of both of mTOR′s downstream targets, p70 ribosomal protein S6 kinase (p70S6 kinase) and 4E-BP1, was also diminished. Overexpression of AKT by AKT cDNA transfection decreased 6-shogaol mediated autophagic cell death, supporting inhibition of AKT beneficial to autophagy. Moreover, reduction of AKT expression by siRNA potentiated 6-shogaol′s effect, also supporting inhibition of AKT beneficial to autophagy. Taken together, these findings suggest that 6-shogaol may be a promising chemopreventive agent against human non-small cell lung cancer. Supramolecular interaction of 6-shogaol, a therapeutic agent of Zingiber officinale with human serum albumin as elucidated by spectroscopic, calorimetric and molecular docking methods PUMID/DOI:DOI: 10.1016/j.phymed.2015.03.016 Phytomedicine. 2015 Jun 1;22(6):621-30. Background: 6-Shogaol, one of the main bioactive constituents of Zingiber officinale has been shown to possess various therapeutic properties. Interaction of a therapeutic compound with plasma proteins greatly affects its pharmacokinetic and pharmacodynamic properties.Purpose: The present investigation was undertaken to characterize the interaction between 6-shogaol and the main in vivo transporter, human serum albumin (HSA).Methods: Various binding characteristics of 6-shogaol-HSA interaction were studied using fluorescence spectroscopy. Thermal stability of 6-shogaol-HSA system was determined by circular dichroisin (CD) and differential scanning calorimetric (DSC) techniques. Identification of the 6-shogaol binding site on HSA was made by competitive drug displacement and molecular docking experiments.Results: Fluorescence quench titration results revealed the association constant, K, of 6-shogaol-HSA interaction as 6.29 +/- 0.33 x 10(4) M-1 at 25 degrees C. Values of the enthalpy change (-11.76 kJ mol(-1)) and the entropy change (52.52 J mol(-1) K-1), obtained for the binding reaction suggested involvement of hydrophobic and van der Waals forces along with hydrogen bonds in the complex formation. Higher thermal stability of HSA was noticed in the presence of 6-shogaol, as revealed by DSC and thermal denaturation profiles. Competitive ligand displacement experiments along with molecular docking results suggested the binding preference of 6-shogaol for Sudlow′s site I of HSA.Conclusion: All these results suggest that 6-shogaol binds to Sudlow′s site I of HSA through moderate binding affinity and involves hydrophobic and van der Waals forces along with hydrogen bonds. (C) 2015 Elsevier GmbH. All rights reserved.


1.0±0.1 g/cm3


Methanol; Acetontrile; Chloroform; DMSO

Flash Point

150.3±19.4 °C

Boiling Point

427.5±35.0 °C at 760 mmHg

Melting Point


InChl Key

WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

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Vascular calcification is the major reason for high mortality of cardiovascular complications for diabetes. Interleukin (IL)-1β has been implicated in this pathogenesis, but its precise role and clinical evidence have not been clearly identified. Hence, this study was aimed to investigate whether high concentration of glucose (HG), which mimics the hyperglycemia environment, could initiate vascular calcification through NLRP3/IL-1β inflammasome and the underlying mechanism. Recently, 6-shogaol, a major ginger derivate, has been elucidated its pharmaceutic role for various diseases. Therefore, the aims of this study also determined 6-shogaol effect in vascular calcification of HG initiation.

Human artery smooth muscle cells (HASMCs) were used in this study. Glucose concentrations at 5 and 25 mM were defined as normal and HG status, respectively. The results showed that HG could increase the NLRP3, cleaved caspase 1, and pro/mature IL-1β levels to induce the expressions of bone-related matrix proteins and subsequent HASMC calcification. This process was regulated by Akt activation and reactive oxygen species (ROS) production. Moreover, 6-shogaol could inhibit the Akt/ROS signaling and NLRP3/caspase 1/IL-1β inflammasome and hence attenuated HASMC calcification.

This study elucidates the detailed mechanism of HG-initiated HASMC calcification through NLRP3/caspase 1/IL-1β inflammasome and indicates a potential therapeutic role of 6-shogaol in vascular calcification complication of diabetes.

© The Author(s) 2020.


6-Shogaol; Interleukin-1β; NLRP3 Inflammasome; Smooth muscle cells; Vascular calcification


The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells.


Chen TC1, Yen CK2, Lu YC2, Shi CS3,4, Hsieh RZ3,5, Chang SF5, Chen CN6.

Publish date

2020 Jan 9




Corrigendum to "6-Shogaol, an active constituent of ginger, attenuates neuroinflammation and cognitive deficits in animal models of dementia" [BBRC 449 (2014) 8-13].


Moon M1, Kim HG2, Choi JG3, Oh H4, Lee PK5, Ha SK6, Kim SY7, Park Y6, Huh Y8, Oh MS9.

Publish date

2020 Jan 8




Periodontitis is an inflammatory disease of the tissues surrounding teeth that causes destruction of connective tissues. During the progress of periodontitis, osteoclasts are solely accountable for the resorption of alveolar bones that leads to the loss of teeth if not properly treated. Thus, the development of effective anti-resorptive therapies will greatly benefit the treatment of periodontitis patients. In the present study, we suggest an inhibitory effect of 6-shogaol, an ingredient of ginger, on osteoclast differentiation and bone resorption. Mouse bone marrow cells were cultured in the presence of macrophage-colony stimulating factor and receptor activator of nuclear factor-κB ligand (RANKL) to investigate the effect of 6-shogaol on osteoclast differentiation and intracellular signaling pathways. 6-shogaol significantly reduced osteoclast differentiation, actin ring formation, and resorption. In the presence of 6-shogaol, osteoclast signaling including the RANKL-induced activation of mitogen-activated protein kinases, Ca2+ oscillation, generation of reactive oxygen species, and nuclear factor of activated T-cells, cytoplasmic 1 nuclear translocation was significantly inhibited in vitro. Furthermore, a ligature-induced periodontitis model in mice was used to determine the role of 6-shogaol in vivo. The administration of 6-shogaol prevented osteoclastogenesis and alveolar bone resorption induced by ligature. Furthermore, the ligature-induced number of macrophages and neutrophils as well as the expression of interleukin-1β and tumor necrosis factor-α were considerably lower in the periodontal tissues following shogaol injection. These results confirm the anti-osteoclastogenic effect of 6-shogaol and suggest the possibility of application as an anti-resorptive strategy in periodontitis.

© 2019 American Academy of Periodontology.


bone resorption; calcium; osteoclasts; periodontitis


6-Shogaol, an active ingredient of ginger, inhibits osteoclastogenesis and alveolar bone resorption in ligature-induced periodontitis in mice.


Kim YG1, Kim MO2, Kim SH3, Kim HJ4, Pokhrel NK4, Lee JH5, Lee HJ6, Kim JY4, Lee Y4.

Publish date

2019 Nov 1