Gypenoside XVII

CAS# 80321-69-3

Gypenoside XVII

Catalog No. BCN2339----Order now to get a substantial discount!

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Quality Control of Gypenoside XVII

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Chemical structure

Gypenoside XVII

3D structure

Chemical Properties of Gypenoside XVII

Cas No. 80321-69-3 SDF Download SDF
PubChem ID 44584555 Appearance White powder
Formula C48H82O18 M.Wt 947.16
Type of Compound Triterpenoids Storage Desiccate at -20°C
Synonyms Gynosaponin S
Solubility DMSO : ≥ 100 mg/mL (105.58 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name (2R,3S,4S,5R,6R)-2-(hydroxymethyl)-6-[[(2R,3S,4S,5R,6S)-3,4,5-trihydroxy-6-[(2S)-2-[(3S,5R,8R,9R,10R,12R,13R,14R,17S)-12-hydroxy-4,4,8,10,14-pentamethyl-3-[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-17-yl]-6-methylhept-5-en-2-yl]oxyoxan-2-yl]methoxy]oxane-3,4,5-triol
SMILES CC(=CCCC(C)(C1CCC2(C1C(CC3C2(CCC4C3(CCC(C4(C)C)OC5C(C(C(C(O5)CO)O)O)O)C)C)O)C)OC6C(C(C(C(O6)COC7C(C(C(C(O7)CO)O)O)O)O)O)O)C
Standard InChIKey ZRBFCAALKKNCJG-SJYBZOGZSA-N
Standard InChI InChI=1S/C48H82O18/c1-22(2)10-9-14-48(8,66-43-40(60)37(57)34(54)27(64-43)21-61-41-38(58)35(55)32(52)25(19-49)62-41)23-11-16-47(7)31(23)24(51)18-29-45(5)15-13-30(44(3,4)28(45)12-17-46(29,47)6)65-42-39(59)36(56)33(53)26(20-50)63-42/h10,23-43,49-60H,9,11-21H2,1-8H3/t23-,24+,25+,26+,27+,28-,29+,30-,31-,32+,33+,34+,35-,36-,37-,38+,39+,40+,41+,42-,43-,45-,46+,47+,48-/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 Gypenoside XVII

The roots of Panax notoginseng (Burk.) F.H.Chen

Biological Activity of Gypenoside XVII

DescriptionGypenoside XVII confers protection against Aβ25-35-induced neurotoxicity through estrogen receptor-dependent activation of PI3K/Akt pathways, inactivation of GSK-3β and activation of Nrf2/ARE/HO-1 pathways. Gypenoside XVII has protective effects to the cellular and rodent models of Alzheimer's disease by activating TFEB.
TargetsBeta Amyloid | PI3K | Akt | GSK-3 | Nrf2 | HO-1 | ARE
In vitro

Attenuation of Aβ25-35-induced parallel autophagic and apoptotic cell death by gypenoside XVII through the estrogen receptor-dependent activation of Nrf2/ARE pathways.[Pubmed: 24726523]

Toxicol Appl Pharmacol. 2014 Aug 15;279(1):63-75.

Amyloid-beta (Aβ) has a pivotal function in the pathogenesis of Alzheimer's disease.
METHODS AND RESULTS:
To investigate Aβ neurotoxicity, we used an in vitro model that involves Aβ25-35-induced cell death in the nerve growth factor-induced differentiation of PC12 cells. Aβ25-35 (20μM) treatment for 24h caused apoptotic cell death, as evidenced by significant cell viability reduction, LDH release, phosphatidylserine externalization, mitochondrial membrane potential disruption, cytochrome c release, caspase-3 activation, PARP cleavage, and DNA fragmentation in PC12 cells. Aβ25-35 treatment led to autophagic cell death, as evidenced by augmented GFP-LC3 puncta, conversion of LC3-I to LC3-II, and increased LC3-II/LC3-I ratio. Aβ25-35 treatment induced oxidative stress, as evidenced by intracellular ROS accumulation and increased production of mitochondrial superoxide, malondialdehyde, protein carbonyl, and 8-OHdG. Phytoestrogens have been proved to be protective against Aβ-induced neurotoxicity and regarded as relatively safe targets for AD drug development. Gypenoside XVII (GP-17) is a novel phytoestrogen isolated from Gynostemma pentaphyllum or Panax notoginseng. Pretreatment with Gypenoside XVII(10μM) for 12h increased estrogen response element reporter activity, activated PI3K/Akt pathways, inhibited GSK-3β, induced Nrf2 nuclear translocation, augmented antioxidant responsive element enhancer activity, upregulated heme oxygenase 1 (HO-1) expression and activity, and provided protective effects against Aβ25-35-induced neurotoxicity, including oxidative stress, apoptosis, and autophagic cell death. In conclusion, Gypenoside XVII conferred protection against Aβ25-35-induced neurotoxicity through estrogen receptor-dependent activation of PI3K/Akt pathways, inactivation of GSK-3β and activation of Nrf2/ARE/HO-1 pathways.
CONCLUSIONS:
This finding might provide novel insights into understanding the mechanism for neuroprotective effects of phytoestrogens or gypenosides.

Enzymatic Biotransformation of Ginsenoside Rb1 and Gypenoside XVII into Ginsenosides Rd and F2 by Recombinant β-glucosidase from Flavobacterium johnsoniae.[Pubmed: 23717145]

J Ginseng Res. 2012 Oct;36(4):418-24.


METHODS AND RESULTS:
This study focused on the enzymatic biotransformation of the major ginsenoside Rb1 into Rd for the mass production of minor ginsenosides using a novel recombinant β-glucosidase from Flavobacterium johnsoniae. The gene (bglF3) consisting of 2,235 bp (744 amino acid residues) was cloned and the recombinant enzyme overexpressed in Escherichia coli BL21(DE3) was characterized. This enzyme could transform ginsenoside Rb1 and Gypenoside XVII to the ginsenosides Rd and F2, respectively. The glutathione S-transferase (GST) fused BglF3 was purified with GST-bind agarose resin and characterized. The kinetic parameters for β-glucosidase had apparent Km values of 0.91±0.02 and 2.84±0.05 mM and Vmax values of 5.75±0.12 and 0.71±0.01 μmol·min(-1)·mg of protein(-1) against p-nitrophenyl-β-D-glucopyranoside and Rb1, respectively. At optimal conditions of pH 6.0 and 37℃, BglF3 could only hydrolyze the outer glucose moiety of ginsenoside Rb1 and Gypenoside XVII at the C-20 position of aglycon into ginsenosides Rd and F2, respectively.
CONCLUSIONS:
These results indicate that the recombinant BglF3 could be useful for the mass production of ginsenosides Rd and F2 in the pharmaceutical or cosmetic industry.

In vivo

Gypenoside XVII Enhances Lysosome Biogenesis and Autophagy Flux and Accelerates Autophagic Clearance of Amyloid-β through TFEB Activation.[Pubmed: 27060963 ]

J Alzheimers Dis. 2016 Apr 5;52(3):1135-50.

A strategy for activating transcription factor EB (TFEB) to restore autophagy flux may provide neuroprotection against Alzheimer's disease. Our previous study reported that Gypenoside XVII (GP-17), which is a major saponin abundant in ginseng and Panax notoginseng, ameliorated amyloid-β (Aβ)25-35-induced apoptosis in PC12 cells by regulating autophagy.
METHODS AND RESULTS:
In the present study, we aimed to determine whether GP-17 has neuroprotective effects on PC12 cells expressing the Swedish mutant of APP695 (APP695swe) and APP/PS1 mice. We also investigated the underlying mechanism. We found that GP-17 could significantly increase Atg5 expression and the conversion of LC3-I to LC3-II in APP695 cells, which was associated with a reduction in p62 expression. GP-17 also elevated the number of LC3 puncta in APP695 cells transduced with pCMV-GFP-LC3. GP-17 promoted the autophagy-based elimination of AβPP, Aβ40, and Aβ42 in APP695swe cells and prevented the formation of Aβ plaques in the hippocampus and cortex of APP/PS1 mice. Furthermore, spatial learning and memory deficits were cured. Atg5 knockdown could abrogate the GP-17-mediated removal of AβPP, Aβ40, and Aβ42 in APP695swe cells. GP-17 upregulated LAMP-1, increased LysoTracker staining, and augmented LAMP-1/LC3-II co-localization. GP-17 could release TFEB from TFEB/14-3-3 complexes, which led to TFEB nuclear translocation and the induction of autophagy and lysosome biogenesis and resulted in the amelioration of autophagy flux. The knockdown of TFEB could abolish these effects of GP-17.
CONCLUSIONS:
In summary, these results demonstrated that GP-17 conferred protective effects to the cellular and rodent models of Alzheimer's disease by activating TFEB.

Protocol of Gypenoside XVII

Structure Identification
Biotechnol Lett. 2014 Jun;36(6):1287-93.

Highly selective hydrolysis for the outer glucose at the C-20 position in ginsenosides by β-glucosidase from Thermus thermophilus and its application to the production of ginsenoside F2 from gypenoside XVII.[Pubmed: 24563303]

β-Glucosidase from Thermus thermophilus has specific hydrolytic activity for the outer glucose at the C-20 position in protopanaxadiol-type ginsenosides without hydrolysis of the inner glucose.
METHODS AND RESULTS:
The hydrolytic activity of the enzyme for Gypenoside XVII was optimal at pH 6.5 and 90 °C, with a half-life of 1 h with 3 g enzyme l(-1) and 4 g Gypenoside XVII l(-1). Under the optimized conditions, the enzyme converted the substrate Gypenoside XVII to ginsenoside F2 with a molar yield of 100 % and a productivity of 4 g l(-1) h(-1). The conversion yield and productivity of ginsenoside F2 are the highest reported thus far among enzymatic transformations.

Appl Microbiol Biotechnol. 2015 Mar 31.

An amino acid at position 512 in β-glucosidase from Clavibacter michiganensis determines the regioselectivity for hydrolyzing gypenoside XVII.[Pubmed: 25820645]

A recombinant β-glucosidase from Clavibacter michiganensis specifically hydrolyzed the outer and inner glucose linked to the C-3 position in protopanaxadiol (PPD)-type ginsenosides and the C-6 position in protopanaxatriol (PPT)-type ginsenosides except for the hydrolysis of gypenoside LXXV (GypLXXV). The enzyme converted Gypenoside XVII (GypXVII) to gypenoside LXXV by hydrolyzing the inner glucose linked to the C-3 position.
METHODS AND RESULTS:
The substrate-binding residues obtained from the Gypenoside XVII-docked homology models of β-glucosidase from C. michiganensis were replaced with alanine, and the amino acid residue at position 512 was selected because of the changed regioselectivity of W512A. Site-directed mutagenesis for the amino acid residue at position 512 was performed. W512A and W512K hydrolyzed the inner glucose linked to the C-3 position and the outer glucose linked to the C-20 position of Gypenoside XVII to produce gypenoside LXXV and F2. W512R hydrolyzed only the outer glucose linked to the C-20 position of Gypenoside XVII to produce F2. However, W512E and W512D exhibited no activity for Gypenoside XVII.
CONCLUSIONS:
Thus, the amino acid at position 512 is a critical residue to determine the regioselectivity for the hydrolysis of Gypenoside XVII. These wild-type and variant enzymes produced diverse ginsenosides, including Gypenoside XVII, GypLXXV, F2, and compound K, from ginsenoside Rb1. To the best of our knowledge, this is the first report of the alteration of regioselectivity on ginsenoside hydrolysis by protein engineering.

Gypenoside XVII Dilution Calculator

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Preparing Stock Solutions of Gypenoside XVII

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.0558 mL 5.2789 mL 10.5579 mL 21.1158 mL 26.3947 mL
5 mM 0.2112 mL 1.0558 mL 2.1116 mL 4.2232 mL 5.2789 mL
10 mM 0.1056 mL 0.5279 mL 1.0558 mL 2.1116 mL 2.6395 mL
50 mM 0.0211 mL 0.1056 mL 0.2112 mL 0.4223 mL 0.5279 mL
100 mM 0.0106 mL 0.0528 mL 0.1056 mL 0.2112 mL 0.2639 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.

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Background on Gypenoside XVII

Gypenoside XVII, a novel phytoestrogen belonging to the gypenosides, can activate estrogen receptors.

In Vitro:The ability of Gypenoside XVII (GP-17) to prevent Ox-LDL-induced cytotoxicity is detected by cell viability assays. Gypenoside XVII does not demonstrate any cytotoxicity in HUVECs. Gypenoside XVII can protect HUVECs against Ox-LDL-induced apoptosis. Gypenoside XVII dose-dependently mitigates the toxic effect of Ox-LDL on HUVEC viability. The viability of HUVECs is significantly higher than that of other groups at 50 μg/mL Gypenoside XVII [1].

In Vivo:Body weights are measured as physical measures of hormone bioactivity. Mean body weights are significantly higher in every group compared to that of the control, but there is no significant difference in body weight between the different treatments during the 10-week feeding. The mouse plasma lipid levels are also measured at the end of 10 weeks of a high-fat diet. Circulating levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) are significantly increased in the treated groups of ApoE-/- mice compared with those of the C57BL/6J control group; Gypenoside XVII (GP-17) and Probucol treatment substantially decreases both of these parameters relative to those of the ApoE-/- model group[1].

References:
[1]. Yang K, et al. Gypenoside XVII Prevents Atherosclerosis by Attenuating Endothelial Apoptosis and Oxidative Stress: Insight into the ERα-Mediated PI3K/Akt Pathway. Int J Mol Sci. 2017 Feb 9;18(2). pii: E77.

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References on Gypenoside XVII

Enzymatic Biotransformation of Ginsenoside Rb1 and Gypenoside XVII into Ginsenosides Rd and F2 by Recombinant beta-glucosidase from Flavobacterium johnsoniae.[Pubmed:23717145]

J Ginseng Res. 2012 Oct;36(4):418-24.

This study focused on the enzymatic biotransformation of the major ginsenoside Rb1 into Rd for the mass production of minor ginsenosides using a novel recombinant beta-glucosidase from Flavobacterium johnsoniae. The gene (bglF3) consisting of 2,235 bp (744 amino acid residues) was cloned and the recombinant enzyme overexpressed in Escherichia coli BL21(DE3) was characterized. This enzyme could transform ginsenoside Rb1 and Gypenoside XVII to the ginsenosides Rd and F2, respectively. The glutathione S-transferase (GST) fused BglF3 was purified with GST-bind agarose resin and characterized. The kinetic parameters for beta-glucosidase had apparent Km values of 0.91+/-0.02 and 2.84+/-0.05 mM and Vmax values of 5.75+/-0.12 and 0.71+/-0.01 mumol.min(-1).mg of protein(-1) against p-nitrophenyl-beta-D-glucopyranoside and Rb1, respectively. At optimal conditions of pH 6.0 and 37, BglF3 could only hydrolyze the outer glucose moiety of ginsenoside Rb1 and Gypenoside XVII at the C-20 position of aglycon into ginsenosides Rd and F2, respectively. These results indicate that the recombinant BglF3 could be useful for the mass production of ginsenosides Rd and F2 in the pharmaceutical or cosmetic industry.

Attenuation of Abeta25-35-induced parallel autophagic and apoptotic cell death by gypenoside XVII through the estrogen receptor-dependent activation of Nrf2/ARE pathways.[Pubmed:24726523]

Toxicol Appl Pharmacol. 2014 Aug 15;279(1):63-75.

Amyloid-beta (Abeta) has a pivotal function in the pathogenesis of Alzheimer's disease. To investigate Abeta neurotoxicity, we used an in vitro model that involves Abeta25-35-induced cell death in the nerve growth factor-induced differentiation of PC12 cells. Abeta25-35 (20muM) treatment for 24h caused apoptotic cell death, as evidenced by significant cell viability reduction, LDH release, phosphatidylserine externalization, mitochondrial membrane potential disruption, cytochrome c release, caspase-3 activation, PARP cleavage, and DNA fragmentation in PC12 cells. Abeta25-35 treatment led to autophagic cell death, as evidenced by augmented GFP-LC3 puncta, conversion of LC3-I to LC3-II, and increased LC3-II/LC3-I ratio. Abeta25-35 treatment induced oxidative stress, as evidenced by intracellular ROS accumulation and increased production of mitochondrial superoxide, malondialdehyde, protein carbonyl, and 8-OHdG. Phytoestrogens have been proved to be protective against Abeta-induced neurotoxicity and regarded as relatively safe targets for AD drug development. Gypenoside XVII (GP-17) is a novel phytoestrogen isolated from Gynostemma pentaphyllum or Panax notoginseng. Pretreatment with GP-17 (10muM) for 12h increased estrogen response element reporter activity, activated PI3K/Akt pathways, inhibited GSK-3beta, induced Nrf2 nuclear translocation, augmented antioxidant responsive element enhancer activity, upregulated heme oxygenase 1 (HO-1) expression and activity, and provided protective effects against Abeta25-35-induced neurotoxicity, including oxidative stress, apoptosis, and autophagic cell death. In conclusion, GP-17 conferred protection against Abeta25-35-induced neurotoxicity through estrogen receptor-dependent activation of PI3K/Akt pathways, inactivation of GSK-3beta and activation of Nrf2/ARE/HO-1 pathways. This finding might provide novel insights into understanding the mechanism for neuroprotective effects of phytoestrogens or gypenosides.

Gypenoside XVII Enhances Lysosome Biogenesis and Autophagy Flux and Accelerates Autophagic Clearance of Amyloid-beta through TFEB Activation.[Pubmed:27060963]

J Alzheimers Dis. 2016 Apr 5;52(3):1135-50.

A strategy for activating transcription factor EB (TFEB) to restore autophagy flux may provide neuroprotection against Alzheimer's disease. Our previous study reported that Gypenoside XVII (GP-17), which is a major saponin abundant in ginseng and Panax notoginseng, ameliorated amyloid-beta (Abeta)25-35-induced apoptosis in PC12 cells by regulating autophagy. In the present study, we aimed to determine whether GP-17 has neuroprotective effects on PC12 cells expressing the Swedish mutant of APP695 (APP695swe) and APP/PS1 mice. We also investigated the underlying mechanism. We found that GP-17 could significantly increase Atg5 expression and the conversion of LC3-I to LC3-II in APP695 cells, which was associated with a reduction in p62 expression. GP-17 also elevated the number of LC3 puncta in APP695 cells transduced with pCMV-GFP-LC3. GP-17 promoted the autophagy-based elimination of AbetaPP, Abeta40, and Abeta42 in APP695swe cells and prevented the formation of Abeta plaques in the hippocampus and cortex of APP/PS1 mice. Furthermore, spatial learning and memory deficits were cured. Atg5 knockdown could abrogate the GP-17-mediated removal of AbetaPP, Abeta40, and Abeta42 in APP695swe cells. GP-17 upregulated LAMP-1, increased LysoTracker staining, and augmented LAMP-1/LC3-II co-localization. GP-17 could release TFEB from TFEB/14-3-3 complexes, which led to TFEB nuclear translocation and the induction of autophagy and lysosome biogenesis and resulted in the amelioration of autophagy flux. The knockdown of TFEB could abolish these effects of GP-17. In summary, these results demonstrated that GP-17 conferred protective effects to the cellular and rodent models of Alzheimer's disease by activating TFEB.

An amino acid at position 512 in beta-glucosidase from Clavibacter michiganensis determines the regioselectivity for hydrolyzing gypenoside XVII.[Pubmed:25820645]

Appl Microbiol Biotechnol. 2015 Oct;99(19):7987-96.

A recombinant beta-glucosidase from Clavibacter michiganensis specifically hydrolyzed the outer and inner glucose linked to the C-3 position in protopanaxadiol (PPD)-type ginsenosides and the C-6 position in protopanaxatriol (PPT)-type ginsenosides except for the hydrolysis of gypenoside LXXV (GypLXXV). The enzyme converted Gypenoside XVII (GypXVII) to GypLXXV by hydrolyzing the inner glucose linked to the C-3 position. The substrate-binding residues obtained from the GypXVII-docked homology models of beta-glucosidase from C. michiganensis were replaced with alanine, and the amino acid residue at position 512 was selected because of the changed regioselectivity of W512A. Site-directed mutagenesis for the amino acid residue at position 512 was performed. W512A and W512K hydrolyzed the inner glucose linked to the C-3 position and the outer glucose linked to the C-20 position of GypXVII to produce GypLXXV and F2. W512R hydrolyzed only the outer glucose linked to the C-20 position of GypXVII to produce F2. However, W512E and W512D exhibited no activity for GypXVII. Thus, the amino acid at position 512 is a critical residue to determine the regioselectivity for the hydrolysis of GypXVII. These wild-type and variant enzymes produced diverse ginsenosides, including GypXVII, GypLXXV, F2, and compound K, from ginsenoside Rb1. To the best of our knowledge, this is the first report of the alteration of regioselectivity on ginsenoside hydrolysis by protein engineering.

Highly selective hydrolysis for the outer glucose at the C-20 position in ginsenosides by beta-glucosidase from Thermus thermophilus and its application to the production of ginsenoside F2 from gypenoside XVII.[Pubmed:24563303]

Biotechnol Lett. 2014 Jun;36(6):1287-93.

beta-Glucosidase from Thermus thermophilus has specific hydrolytic activity for the outer glucose at the C-20 position in protopanaxadiol-type ginsenosides without hydrolysis of the inner glucose. The hydrolytic activity of the enzyme for Gypenoside XVII was optimal at pH 6.5 and 90 degrees C, with a half-life of 1 h with 3 g enzyme l(-1) and 4 g Gypenoside XVII l(-1). Under the optimized conditions, the enzyme converted the substrate Gypenoside XVII to ginsenoside F2 with a molar yield of 100 % and a productivity of 4 g l(-1) h(-1). The conversion yield and productivity of ginsenoside F2 are the highest reported thus far among enzymatic transformations.

Description

Gypenoside XVII, a novel phytoestrogen belonging to the gypenosides, can activate estrogen receptors.

Keywords:

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