Ginger Studies Anti-inflammation Anti-cancer
gingerols and 6-shogaols
anti-ulcer, protect mucus
Anti-cancer via ROS, caspases activation, inhibition of MMP-9 via blockage of NF-kB signaling
6-shogaol inhibits microtubules
inhibiting TRAIL-induced NF-kappaB activation while 6-shogaol alone reduces viability by damaging microtubules.
reducing MMP-9 expression and secretion
6-shogaol inhibits NFkB
6-shogaol exerts an anti-inflammatory effect through down-regulation of NF-百B signalling
gingerols enhance glucose uptake by increasing surface GLUT4
Front Cell Infect Microbiol. 2018 Aug 28;8:299. doi:
10.3389/fcimb.2018.00299. eCollection 2018.
Antibiofilm and Antivirulence Activities of 6-Gingerol and 6-Shogaol Against Candida albicans Due to Hyphal Inhibition.
Lee JH1, Kim YG1, Choi P2, Ham J2, Park JG3, Lee J1.
School of Chemical Engineering, Yeungnam University, Gyeongsan, South Korea.
Natural Products Research Institute, Korea Institute of Science and Technology, Gangneung, South Korea.
Advanced Bio Convergence Center, Pohang Technopark Foundation, Pohang, South Korea.
Candida albicans is an opportunistic pathogen and responsible for candidiasis. C. albicans readily forms biofilms on various biotic and abiotic surfaces, and these biofilms can cause local and systemic infections. C. albicans biofilms are more resistant than its free yeast to antifungal agents and less affected by host immune responses. Transition of yeast cells to hyphal cells is required for biofilm formation and is believed to be a crucial virulence factor. In this study, six components of ginger were investigated for antibiofilm and antivirulence activities against a fluconazole-resistant C. albicans strain. It was found 6-gingerol, 8-gingerol, and 6-shogaol effectively inhibited biofilm formation. In particular, 6-shogaol at 10 米g/ml significantly reduced C. albicans biofilm formation but had no effect on planktonic cell growth. Also, 6-gingerol and 6-shogaol inhibited hyphal growth in embedded colonies and free-living planktonic cells, and prevented cell aggregation. Furthermore, 6-gingerol and 6-shogaol reduced C. albicans virulence in a nematode infection model without causing toxicity at the tested concentrations. Transcriptomic analysis using RNA-seq and qRT-PCR showed 6-gingerol and 6-shogaol induced several transporters (CDR1, CDR2, and RTA3), but repressed the expressions of several hypha/biofilm related genes (ECE1 and HWP1), which supported observed phenotypic changes. These results highlight the antibiofilm and antivirulence activities of the ginger components, 6-gingerol and 6-shogaol, against a drug resistant C. albicans strain.
C. albicans; antivirulence; biofilm; gingerol; hyphae; shogaol
6-Shogaol, an active constituent of ginger, inhibits breast cancer cell invasion by reducing matrix metalloproteinase-9 expression via blockade of nuclear factor-百B activation
H Ling, H Yang, [...], and E-H Chew
Additional article information
BACKGROUND AND PURPOSE
Shogaols are reported to possess anti-inflammatory and anticancer activities. However, the antimetastatic potential of shogaols remains unexplored. This study was performed to assess the effects of shogaols against breast cancer cell invasion and to investigate the underlying mechanisms.
The anti-invasive effect of a series of shogaols was initially evaluated on MDA-MB-231 breast cancer cells using the matrigel invasion assay. The suppressive effects of 6-shogaol on phorbol 12-myristate 13-acetate (PMA)-induced matrix metalloproteinase-9 (MMP-9) gelatinolytic activity and nuclear factor-百B (NF-百B) activation were further determined.
NF-百B has been suggested to be a target for many biologically active natural products derived from plant foods such as curcumin, resveratrol, epigallocatechin gallate and sulforaphane (Surh et al., 2001; Woo et al., 2004). Moreover, studies have reported that 6-shogaol exerts an anti-inflammatory effect through down-regulation of NF-百B signalling (Pan et al., 2008a). However, to date, the molecular mechanism by which 6-shogaol inhibits the NF-百B activation cascade is not fully understood. Our present study had demonstrated that 6-shogaol exerted anti-NF-百B effect through inhibition of phosphorylation of IKK汐 and IKK汕 subunits of the IKK complex. This led to blockade of I百B汐 phosphorylation and prevention of I百B汐 proteosomal degradation with a resulting decrease in p65 nuclear translocation and NF-百B transcriptional activation. Furthermore, 6-shogaol inhibited p65 phosphorylation at serine 536 without affecting total p65 expression. The phosphorylation of p65 at serine 536 has been suggested to play an important role in p65 nuclear localization and transcriptional activity (Ghosh and Karin, 2002; Viatour et al., 2005). Taken together, our findings demonstrate that the in vitro anti-invasive effect of 6-shogaol is mediated through its interference with NF-百B signalling.
In summary, our study has focused on the naturally occurring shogaols found in ginger. We have demonstrated that sublethal doses of 6-, 8- and 10-shogaol, by reducing MMP-9 expression and secretion, have an inhibitory effect on PMA-induced breast cancer cell invasion. Furthermore, we provide evidence that 6-shogaol impairs breast cancer cell invasion, at least in part, through targeting the NF-百B activation cascade (summarized in Figure 7). In recent years, an increasing number of natural products possessing anticancer properties have been unveiled. Coupled with the elucidation of their antitumour mechanism(s), the exploitation of their use in clinical chemotherapeutic strategies is promisingly realizing. In view of the impressive in vitro potency of 6-shogaol in reversing PMA-induced cancer cell invasion at non-cytotoxic concentrations, and as specific antimetastatic agents with minimal or no complications from their cytotoxicities are preferred, this series of naturally occurring phytochemicals are indeed worthy of further development as antimetastatic agents for clinical use.
6-Shogaol, an active constituent of ginger, inhibits breast cancer cell invasion by reducing matrix metalloproteinase-9 expression via blockade of nuclear factor-百B activation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3010581/
6-Shogaol & 6-Gingerol
2 November 2015
[ Excerpts ]
NEW STUDY SHOWS GINGER IS 10,000X STRONGER THAN CHEMO (AND ONLY KILLS CANCER CELLS)
[ A study conducted by Georgia State University found that 6-Shogaol ( extract of ginger ) reduced mouse prostate tumor size by 56%... Another study showed it to be superior to chemotherapy against breast cancer stem cells, at concentrations that are non-toxic to normal cells. 6-shogaol increases apoptosis -- cancer cell death -- by inducing of autophagy, and it inhibits the formaton of breast cancer lumps... The cancer drug taxol is not nearly as effective as 6-shogaol, which is 10,000 times more effective at killing cancer stem cells, inhibits tumor formation, and prevents the formation of tumors. ]
Shogaol, also known as (6)-shogaol, is a pungent
constituent of ginger similar in chemical structure to gingerol. Like zingerone,
it is produced when ginger is dried or cooked.
Shogaols are artifacts formed during storage or through excess heat, probably created by a dehydration reaction of the gingerols. The ratio of shogaols to gingerols sometimes is taken as an indication of product quality.
The name 'shogaol' is derived from the Japanese name for ginger (汜蔽﹜sh身ga).
Shogaol is rated 160,000 SHU on Scoville scale. When compared to other pungent compounds, shogaol is moderately more pungent than piperine, but less than capsaicin.
Compound Scoville Heat Units (SHU)
Among ginger constituents, it has a very strong antitussive (anti-cough) effect.[medical citation needed] Both shogaol and gingerols reduced blood pressure and gastric contraction. Shogaol has been shown to induce apoptosis (kill) in human colorectal carcinoma cells via reactive oxygen species. It is broken down into 16 metabolites via the mercapturic acid pathway. Acetylcysteine was found to reduce effectiveness of shogaol's apoptotic properties.
6-Shogaol ( Extract of Ginger ) vs Cancer http://www.rexresearch.com/6shogaol/6shogaol.html
Biochem Biophys Res Commun. 2007 Oct 12;362(1):218-23. Epub 2007 Aug 10.
Ginger ingredients reduce viability of gastric cancer cells via distinct mechanisms.
Ishiguro K, Ando T, Maeda O, Ohmiya N, Niwa Y, Kadomatsu K, Goto H.
Ginger has been used throughout the world as spice, food and traditional herb. We found that 6-gingerol, a phenolic alkanone isolated from ginger, enhanced the TRAIL-induced viability reduction of gastric cancer cells while 6-gingerol alone affected viability only slightly. 6-Gingerol facilitated TRAIL-induced apoptosis by increasing TRAIL-induced caspase-3/7 activation. 6-Gingerol was shown to down-regulate the expression of cIAP1, which suppresses caspase-3/7 activity, by inhibiting TRAIL-induced NF-kappaB activation. As 6-shogaol has a chemical structure similar to 6-gingerol, we also assessed the effect of 6-shogaol on the viability of gastric cancer cells. Unlike 6-gingerol, 6-shogaol alone reduced the viability of gastric cancer cells. 6-Shogaol was shown to damage microtubules and induce mitotic arrest. These findings indicate for the first time that in gastric cancer cells, 6-gingerol enhances TRAIL-induced viability reduction by inhibiting TRAIL-induced NF-kappaB activation while 6-shogaol alone reduces viability by damaging microtubules.
J. Agric. Food Chem., 2015, 63 (6), pp 1730每1738
February 9, 2015
6-Shogaol, an Active Constituent of Dietary Ginger, Impairs Cancer Development and Lung Metastasis...
Ya-Ling Hsu, Jen-Yu Hung, Ying-Ming Tsai, Eing-Mei Tsai, Ming-Shyan Huang, Ming-Feng Hou, and Po-Lin Kuo
This study has two novel findings: it is not only the first to demonstrate that tumor-associated dendritic cells (TADCs) facilitate lung and breast cancer metastasis in vitro and in vivo by secreting inflammatory mediator CC-chemokine ligand 2 (CCL2), but it is also the first to reveal that 6-shogaol can decrease cancer development and progression by inhibiting the production of TADC-derived CCL2. Human lung cancer A549 and breast cancer MDA-MB-231 cells increase TADCs to express high levels of CCL2, which increase cancer stem cell features, migration, and invasion, as well as immunosuppressive tumor-associated macrophage infiltration. 6-Shogaol decreases cancer-induced up-regulation of CCL2 in TADCs, preventing the enhancing effects of TADCs on tumorigenesis and metastatic properties in A549 and MDA-MB-231 cells. A549 and MDA-MB-231 cells enhance CCL2 expression by increasing the phosphorylation of signal transducer and activator of transcription 3 (STAT3), and the activation of STAT3 induced by A549 and MDA-MB-231 is completely inhibited by 6-shogaol. 6-Shogaol also decreases the metastasis of lung and breast cancers in mice. 6-Shogaol exerts significant anticancer effects on lung and breast cells in vitro and in vivo by targeting the CCL2 secreted by TADCs. Thus, 6-shogaol may have the potential of being an efficacious immunotherapeutic agent for cancers.
6-Shogaol ( Extract of Ginger ) vs Cancer http://www.rexresearch.com/6shogaol/6shogaol.html
Metabolism of -Shogaol in Mice and in Cancer Cells
Huadong Chen, Lishuang Lv, Dominique Soroka, Renaud
F. Warin, Tiffany A. Parks, Yuhui Hu, Yingdong Zhu, Xiaoxin Chen and Shengmin
Sang Abstract Ginger has received extensive attention because of its
antioxidant, anti-inflammatory, and antitumor activities. However, the metabolic
fate of its major components is still unclear. In the present study, the
metabolism of -shogaol, one of the major active components in ginger, was
examined for the first time in mice and in cancer cells. Thirteen metabolites
were detected and identified, seven of which were purified from fecal samples
collected from -shogaol-treated mice. Their structures were elucidated as
1-(4∩-hydroxy-3∩-methoxyphenyl)-decan-3-one (M11), and
5-methylthio-1-(4∩-hydroxy-3∩-methoxyphenyl)-decan-3-ol (M12) on the basis of
detailed analysis of their 1H, 13C, and two-dimensional NMR data. The rest of
the metabolites were identified as 5-cysteinyl-M6 (M1), 5-cysteinyl--shogaol
(M2), 5-cysteinylglycinyl-M6 (M3), 5-N-acetylcysteinyl-M6 (M4),
5-N-acetylcysteinyl--shogaol (M5), and 5-glutathiol--shogaol (M13) by
analysis of the MSn (n = 1每3) spectra and comparison to authentic standards.
Among the metabolites, M1 through M5, M10, M12, and M13 were identified as the
thiol conjugates of -shogaol and its metabolite M6. M9 and M11 were
identified as the major metabolites in four different cancer cell lines
(HCT-116, HT-29, H-1299, and CL-13), and M13 was detected as a major metabolite
in HCT-116 human colon cancer cells. We further showed that M9 and M11 are
bioactive compounds that can inhibit cancer cell growth and induce apoptosis in
human cancer cells. Our results suggest that 1) -shogaol is extensively
metabolized in these two models, 2) its metabolites are bioactive compounds, and
3) the mercapturic acid pathway is one of the major biotransformation pathways
of -shogaol. ＃Shogaols have gained interest because of recent discoveries
revealing their higher anticancer potencies over gingerols. It is reported that
-, -, and -gingerols had little to no effect but -shogaol
significantly inhibited the growth of A-2780 ovarian cancer cells (Rhode et al.,
2007). Kim et al. (2008) reported that -shogaol exhibited much stronger
growth-inhibitory effects on A-549 human lung cancer cells, SK-OV-3 human
ovarian cancer cells, SKMEL-2 human skin cancer cells, and HCT-15 human colon
cancer cells than -, -, -, and -gingerols. A study from our group
has also demonstrated that -, -, and -shogaols exhibited much higher
antiproliferative potency than -, -, and -gingerols against H-1299
human lung cancer cells with IC50 values of 8 米M for -shogaol and 150 米M for
-gingerol (Sang et al., 2009). Along with our collaborators, we have reported
that -shogaol was more effective than -gingerol in inhibiting
12-O-tetradecanoylphorbol-13-acetate-induced tumor promotion in mice (Wu et al.,
2010). Furthermore, Dugasani et al. (2010) found that -shogaol showed the
most potent antioxidative activity with an IC50 value of approximately 8 米M,
whereas -, -, and -gingerols had IC50 values of 28, 20, and 12 米M,
Br J Pharmacol. 2010 Dec; 161(8): 1763每1777.
6-Shogaol, an active constituent of ginger, inhibits breast cancer cell invasion...
Shogaols (6-, 8- and 10-shogaol) inhibited PMA-stimulated MDA-MB-231 cell invasion with an accompanying decrease in MMP-9 secretion. 6-Shogaol was identified to display the greatest anti-invasive effect in association with a dose-dependent reduction in MMP-9 gene activation, protein expression and secretion. The NF-百B transcriptional activity was decreased by 6-shogaol; an effect mediated by inhibition of I百B phosphorylation and degradation that subsequently led to suppression of NF-百B p65 phosphorylation and nuclear translocation. In addition, 6-shogaol was found to inhibit JNK activation with no resulting reduction in activator protein-1 transcriptional activity. By using specific inhibitors, it was demonstrated that ERK and NF-百B signalling, but not JNK and p38 signalling, were involved in PMA-stimulated MMP-9 activation.
CONCLUSIONS AND IMPLICATIONS
6-Shogaol is a potent inhibitor of MDA-MB-231 cell invasion, and the molecular mechanism involves at least in part the down-regulation of MMP-9 transcription by targeting the NF-百B activation cascade. This class of naturally occurring small molecules thus have potential for clinical use as antimetastatic treatments.
Toxicology and applied pharmacology 2014
Gingerol sensitizes TRAIL-induced apoptotic cell death of glioblastoma cells
Dae-Hee Lee, Dong-Wook Kim, [...], and Daeho Park
Additional article information
Glioblastoma multiforme (GBM) is the most lethal and aggressive astrocytoma of primary brain tumors in adults. Although there are many clinical trials to induce the cell death of glioblastoma cells, most glioblastoma cells have been reported to be resistant to TRAIL-induced apoptosis. Here, we showed that gingerol as a major component of ginger can induce TRAIL-mediated apoptosis of glioblastoma. Gingerol increased death receptor (DR) 5 levels in a p53-dependent manner. Furthermore, gingerol decreased the expression level of anti-apoptotic proteins (survivin, c-FLIP, Bcl-2, and XIAP) and increased pro-apoptotic protein, Bax and truncate Bid, by generating reactive oxygen species (ROS).We also found that the sensitizing effects of gingerol in TRAIL-induced cell death were blocked by scavenging ROS or overexpressing anti-apoptotic protein (Bcl-2). Therefore, we showed the functions of gingerol as a sensitizing agent to induce cell death of TRAIL-resistant glioblastoma cells. This study gives rise to the possibility of applying gingerol as an anti-tumor agent that can be used for the purpose of combination treatment with TRAIL in TRAIL-resistant glioblastoma tumor therapy.
Keywords: Gingerol, Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), Glioblastoma, Apoptosis, Reactive oxygen species (ROS), p53
Glioblastoma multiforme (GBM) is classified as a grade IV astrocytoma by the World Health Organization (WHO) and is a very aggressive malignant astrocytoma that makes up approximately 50% of all astrocytomas (Fuller, 2008; Ohgaki and Kleihues, 2005). As it is known from its name, GBM has morphologically multiple heterogeneous populations (Krakstad and Chekenya, 2010). Although there have been many radiotherapeutic and chemotherapeutic clinical trials to treat glioblastoma, prognosis of glioblastoma patients is very poor and the median survival rate is about 14.6 months (Stupp et al., 2005). Recently, combination therapies such as cocktail treatments that use more than 2 different anti-cancer drugs have been tried to increase the efficacy and survival rate (Doherty et al., 2006; Goudar et al., 2005; Rao et al., 2005; Reardon et al., 2006). For example, drugs that target both survival pathway and apoptotic pathway have simultaneously been used to improve the survival rate for GBM patients (Hawkins, 2004; Krakstad and Chekenya, 2010).
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has been well known to mediate cellular apoptosis in a wide-range of tumor cell types (Aggarwal, 2003; Pitti et al., 1996). TRAIL binds to its receptor (death receptor (DR) 4/5) to induce receptor trimerization that can recruit downstream molecules such as Fas-associated protein with death domain (FADD) and eventually activate caspase cascade (caspases-8, 10, 9, and 3) to transmit cell death signaling (Aggarwal, 2003; Bellail et al., 2010). However, it has been reported that most glioblastoma cells showed resistance to apoptosis mediated by the TRAIL signaling pathway (Krakstad and Chekenya, 2010).
Gingerol, as a major pungent element of ginger, has been reported to exhibit anti-oxidant, analgesic, anti-pyretic, anti-inflammatory, and anti-tumorigenic activities (Oyagbemi et al., 2010; Shukla and Singh, 2007). Gingerol has also been known to show anti-inflammatory potential by decreasing the expression level of inducible nitric oxide synthase (iNOS) and TNF-汐 (D.H. Lee et al., 2009; T.Y. Lee et al., 2009). Furthermore, the anti-tumorigenic effects of gingerol have been known to be exerted by the induction of apoptosis of tumor cells (Bode et al., 2001; Chakraborty et al., 2012; Lee and Surh, 1998). However, the detailed molecular mechanism of gingerol-induced apoptosis is still not clear.
Here, we identified that gingerol functions as a sensitizing agent to induce TRAIL-mediated apoptosis of glioblastoma cells which were resistant to apoptosis by TRAIL signaling. Especially, in non-cytotoxic concentrations gingerol efficiently induced cell death by TRAIL in glioblastoma cell lines. Furthermore, we revealed that the sensitizing function of gingerol was performed by elevating the expression level of death receptor (DR) 5, by decreasing the expression of anti-apoptotic proteins (survivin, c-FLIP, Bcl-2, and XIAP) and by inducing the levels of pro-apoptotic proteins (Bax and truncate Bid) in a p53- and reactive oxygen species (ROS)-dependent manner. Our effort in identifying gingerol as the agent that sensitizes TRAIL-mediated apoptosis in glioblastoma and understanding the molecular mechanisms of gingerol-sensitization provides us which an opportunity to make more effective drug combination therapies which are non-toxic to GBM patients.
Gingerol sensitizes TRAIL-induced apoptotic cell death of
Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) Pathway
Department of Pharmacology and University of Colorado Comprehensive Cancer Center, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado
Journal of Thoracic Oncology
Volume 2, Issue 6, June 2007, Pages 461-465
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/Apo1L is a death ligand, a cytokine that activates apoptosis through cell surface death receptors. TRAIL is thought to be important in host tumor surveillance and metastasis suppression, and various therapeutic agonists that activate TRAIL receptors to induce tumor cell apoptosis are in clinical development. This review discusses recent findings about TRAIL pathway signaling and relates the signaling mechanisms to issues that need to be considered as we try to manipulate TRAIL signaling to treat cancer.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL, also known as Apo2L and TNFSF10) is a type II transmembrane protein belonging to the tumor necrosis factor (TNF) superfamily. TRAIL is expressed on the surface of natural killer (NK) and T cells, macrophages, and dendritic cells. As with other cytokines, the protein is synthesized in a pro-form with a signal sequence that is removed in the mature secreted protein. TRAIL can be anchored in the membrane via hydrophobic amino acids or can be released as a soluble protein. Both forms function as trimers and can induce apoptosis. TRAIL induces apoptosis by binding to and activating signaling by trimeric death receptors in a manner that is similar to that of other ※death ligands,求 such as FasL or TNF汐, which signal through the Fas receptor (CD95) and TNF receptor (TNFR1), respectively. TRAIL binds to five different receptors. DR4 (TNFRSF10a, TRAILR1) and DR5 (TNFRSF10b, TRAILR2) are both are capable of signaling apoptosis, whereas two membrane-bound decoy receptors called DcR1 (TNFRSF10c) and DcR2 (TNFRSF10d) are unable to activate apoptotic signaling and inhibit TRAIL signaling. The fifth TRAIL-binding receptor is osteoprotogerin (TNFRSF11b), which is a soluble protein that may also function as a decoy/inhibitor by sequestering TRAIL extracellularly. Much current interest in TRAIL derives from its roles in cancer development and treatment. In particular, recombinant TRAIL1, 2 and agonistic antibodies that recognize TRAIL receptors3, 4 have been shown to kill many tumor cells while leaving most normal cells unscathed and displaying little toxicity when delivered systemically to animals and people. It is therefore hoped that these agents may be useful to treat cancer.5, 6, 7 This contrasts with other death ligands, such as TNF汐 or Fas ligand, which activate similar pathways using the same signaling proteins but display unacceptable toxicity when administered systemically.
FUNCTIONS OF TRAIL
The creation of TRAIL-deficient and TRAIL receptor-deficient mice has allowed examination of the physiological functions of TRAIL. Knockout mice are viable and fertile with no obvious developmental defects. The TRAIL pathway is involved in the regulation of innate immunity8 and in the homeostasis of memory T cells.9 From the cancer perspective, TRAIL signaling is important in T cell- and natural killer cell-mediated tumor surveillance and metastasis suppression.10, 11, 12, 13 Although TRAIL receptor deficiency has no apparent effect on intestinal tumor development caused by p53 or APC loss,14 TRAIL-deficient animals have more hematological malignancies15 and are more susceptible to chemical carcinogens.13 TRAIL receptor-deficient animals are also less sensitive to damage caused by ionizing radiation.16 Together, these findings indicate that the TRAIL pathway has important roles in host anti-tumor defense and tumor suppression.
Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) Pathway
Signaling - ScienceDirect
Planta Med. 2012 Sep;78(14):1549-55. Epub 2012 Jul 24.
Gingerols of Zingiber officinale enhance glucose uptake by increasing cell surface GLUT4 in cultured L6 myotubes.
Li Y1, Tran VH, Duke CC, Roufogalis BD.
Faculty of Pharmacy, The University of Sydney, Sydney, Australia.
In this study we investigate the active constituents of the rhizome of Zingiber officinale, Roscoe (ginger) and determine their activity on glucose uptake in cultured L6 myotubes and the molecular mechanism underlying this action. Freeze-dried ginger powder was extracted with ethyl acetate (1 kg/3 L) to give the total ginger extract, which was then separated into seven fractions, consisting of nonpolar to moderately polar compounds, using a short-column vacuum chromatographic method. The most active fraction (F7) was further purified for identification of its active components. The effect of the extract, fractions, and purified compounds on glucose uptake was evaluated using radioactive labelled 2-[1,2-³H]-deoxy-D-glucose in L6 myotubes. The pungent phenolic gingerol constituents were identified as the major active compounds in the ginger extract enhancing glucose uptake. (S)--Gingerol was the most abundant component among the gingerols, however, (S)--gingerol was the most potent on glucose uptake. The activity of (S)--gingerol was found to be associated primarily with an increase in surface distribution of GLUT4 protein on the L6 myotube plasma membrane, as detected by expression of hemagglutinin epitope-tagged GLUT4 in L6 muscle cells. The enhancement of glucose uptake in L6 rat skeletal muscle cells by the gingerol pungent principles of the ginger extract supports the potential of ginger and its pungent components for the prevention and management of hyperglycemia and type 2 diabetes.
Georg Thieme Verlag KG Stuttgart ﹞ New York.
Gingerols of Zingiber officinale enhance glucose uptake by increasing cell
surface GLUT4 in cultured L6 myotubes. - PubMed - NCBI