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Gypenoside A Sale

(Synonyms: 七叶胆苷 A;绞股蓝皂苷 A) 目录号 : GC36204

Gypenoside A 是从绞股蓝中分离得到的天然产物。

Gypenoside A Chemical Structure

Cas No.:157752-01-7

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产品描述

Gypenoside A is a natural compound isolaated from Gynostemma pentaphyllum Makino[1].

[1]. Liu G, et al. Determination on the glycosyl sequence of gypenoside A by TLC-FABMS. Zhong Yao Cai. 1997 Aug;20(8):398-400.

Chemical Properties

Cas No. 157752-01-7 SDF
别名 七叶胆苷 A;绞股蓝皂苷 A
Canonical SMILES O=CC12C3C(C4(C(C(C5(CC(/C=C(C)/C)OC5O)O)CC4)CC3)C)(CCC1C(C)(C(OC6C(C(C(O)CO6)OC7C(C(C(O)CO7)O)O)OC8C(C(C(O)C(C)O8)O)O)CC2)C)C
分子式 C46H74O17 分子量 899.07
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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1 mM 1.1123 mL 5.5613 mL 11.1226 mL
5 mM 0.2225 mL 1.1123 mL 2.2245 mL
10 mM 0.1112 mL 0.5561 mL 1.1123 mL
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Research Update

Determination of Gypenoside A and Gypenoside XLIX in Rat Plasma by UPLC-MS/MS and Applied to the Pharmacokinetics and Bioavailability

Int J Anal Chem 2022 Aug 12;2022:6734408.PMID:35992562DOI:10.1155/2022/6734408.

In this work, a UPLC-MS/MS method was developed for the determination of Gypenoside A and gypenoside XLIX in rat plasma. For chromatographic separation, a UPLC BEH C18 column was employed, the mobile phase comprised acetonitrile: water (w/0.1% formic acid), and the elution time was 4 min. Detection of each compound was enabled by electrospray ionization in negative-ion mode, and quantitative analysis was enabled by operating in multiple reaction monitoring (MRM) mode by monitoring the transitions of m/z 897.5⟶403.3 for Gypenoside A, m/z 1045.5⟶118.9 for gypenoside XLIX, and m/z 825.4⟶617.5 for the internal standard. The calibration curves for Gypenoside A and gypenoside XLIX demonstrated excellent linearity (r > 0.995) over the range of 2-3000 ng/mL. The intraday and interday precisions of Gypenoside A and gypenoside XLIX were within 14.9%, the intraday and interday accuracies ranged from 90.1% to 113.9%, the recoveries were all greater than 88.3%, and the matrix effect ranged from 87.1% to 94.1%. The developed method was successfully applied in the determination of the pharmacokinetics of Gypenoside A and gypenoside XLIX. Gypenoside A and gypenoside XLIX had very short half-lives in rats, with oral t 1/2z of 1.4 ± 0.2 h and 1.8 ± 0.6 h, respectively, and low bioavailabilities (0.90% and 0.14%, respectively).

Gypenoside A from Gynostemma pentaphyllum Attenuates Airway Inflammation and Th2 Cell Activities in a Murine Asthma Model

Int J Mol Sci 2022 Jul 12;23(14):7699.PMID:35887041DOI:10.3390/ijms23147699.

Our previous study found that oral administration of Gynostemma pentaphyllum extract can attenuate airway hyperresponsiveness (AHR) and reduce eosinophil infiltration in the lungs of asthmatic mice. Gypenoside A is isolated from G. pentaphyllum. In this study, we investigated whether Gypenoside A can effectively reduce asthma in mice. Asthma was induced in BALB/c mice by ovalbumin injection. Asthmatic mice were treated with Gypenoside A via intraperitoneal injection to assess airway inflammation, AHR, and immunomodulatory effects. In vitro, Gypenoside A reduced inflammatory and oxidative responses in inflammatory tracheal epithelial cells. Experimental results showed that Gypenoside A treatment can suppress eosinophil infiltration in the lungs, reduce tracheal goblet cell hyperplasia, and attenuate AHR. Gypenoside A significantly reduced Th2 cytokine expression and also inhibited the expression of inflammatory genes and proteins in the lung and bronchoalveolar lavage fluid. In addition, Gypenoside A also significantly inhibited the secretion of inflammatory cytokines and chemokines and reduced oxidative expression in inflammatory tracheal epithelial cells. The experimental results suggested that Gypenoside A is a natural compound that can effectively reduce airway inflammation and AHR in asthma, mainly by reducing Th2 cell activation.

Gypenoside A attenuates dysfunction of pancreatic β cells by activating PDX1 signal transduction via the inhibition of miR-150-3p both in vivo and in vitro

J Biochem Mol Toxicol 2022 Apr;36(4):e23004.PMID:35191145DOI:10.1002/jbt.23004.

Saponin Gypenoside A (GP) has shown its potential to handle diabetes mellitus. MicroRNA-150-3p (miR-150-3p) is closely related to the dysfunction of pancreatic β cells by targeting PDX1. Given the function of GP is related to its regulation on different miRs, the current study assessed the role of miR-150-3p as a therapeutic target for the hypoglycemic effects of GP. Pancreatic β cell dysfunction was induced in mice using the high-fatty diet (HFD) method and then handled with GP. Changes in insulin release and resistance and the activity of the miR-150-3p/PDX1 axis were detected. The expression of miR-150-3p was induced to confirm its central in the effects of GP. The results of in vivo tests were then validated with in vitro assays. HFD administration suppressed glucose tolerance, delayed insulin release, and induced insulin resistance and pancreas apoptosis in mice, which was indicative of the dysfunction of β pancreatic cells. Changes in pancreatic β function were associated with the increased expression of miR-150-3p and suppressed expression of PDX1. After the administration of GP, the impairments of the pancreas were alleviated and the expression of miR-150-3p was inhibited, contributing to the restored level of PDX1. The injection of miR-150-3p agomir counteracted the protective effects of GP. In in vitro assays, the pretransfection of miR-150-3p mimetics also counteracted the protective effects of GP on pancreatic β cells against palmitic acid. Collectively, miR-150-3p played a key role in the protective effects of GP against pancreatic β cell dysfunction by inhibiting PDX1 expression.

Gypenoside A protects ischemia/reperfusion injuries by suppressing miR-143-3p level via the activation of AMPK/Foxo1 pathway

Biofactors 2020 May;46(3):432-440.PMID:31889343DOI:10.1002/biof.1601.

Ischemia-reperfusion (I/R) injury is a major side effect associated with coronary heart disease (CHD). Gypenoside A (GP) is one of the dominant active components of Gynostemma pentaphyllum and has the potential to attenuate myocardial I/R injuries. The major purpose of this study was to explore the mechanism driving the protective effect of GP on myocardial tissue by focusing on the interaction between GP and miR-143-3p. Cardiomyocytes were pre-treated with GP and subjected to oxygen-glucose deprivation/re-oxygenation (OGD/R). Changes in cell viability, apoptosis, and expression levels of factors involved in the adenosine monophosphate activated protein kinase (AMPK)/Foxo1-mediated miR-143-3p pathway were detected. The levels of AMPK and miR-143-3p were then modulated using an inhibitor and a mimic, respectively, to confirm their central roles in the effect of GP. The administration of GP attenuated OGD/R-induced injuries by increasing cell viability and suppressing apoptosis, which was associated with the activation of AMPK/Foxo1 signaling and the decreased level of miR-143-3p. The down-regulation of AMPK and up-regulation of miR-143-3p both counteracted the function of GP on cardiomyocytes. The role of miR-143-3p suppression in the anti-I/R effect of GP was also verified with rat model. The injection of miR-143-3p agomir inhibited the cardio-protective effect of GP in a manner similar to that in the in vitro assays. Our results confirm the cardio-protective effect of GP, which is exerted by suppressing the level of miR-143-3p via the activation of AMPK signaling.

Development of a targeted method for quantification of gypenoside XLIX in rat plasma, using SPE and LC-MS/MS

Biomed Chromatogr 2017 Jun;31(6).PMID:27859537DOI:10.1002/bmc.3898.

A sensitive, selective and rapid liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed for the quantification of gypenoside XLIX, a naturally occurring gypenoside of Gynostemma pentaphyllum in rat plasma and then validated according to the US Food and Drug Administration's Guidance for Industry: Bioanalytical Method Validation. Plasma samples were prepared by a simple solid-phase extraction. Separation was performed on a Waters XBridgeTM BEH C18 chromatography column (4.6 × 50 mm, 2.5 μm) using a mobile phase of acetonitrile and water (62.5:37.5, v/v). Gypenoside XLIX and the internal standard Gypenoside A were detected in the negative ion mode using selection reaction monitoring of the transitions at m/z 1045.6 → 913.5 and 897.5 → 765.4, respectively. The calibration curve was linear (R2 > 0.990) over a concentration range of 10-7500 ng/mL with the lower quantification limit of 10 ng/mL. Intra- and inter-day precision was within 8.6% and accuracy was ≤10.2%. Stability results proved that gypenoside XLIX and the IS remained stable throughout the analytical procedure. The validated LC-MS/MS method was then applied to analyze the pharmacokinetics of gypenoside XLIX after intravenous administration to rats (1.0, 2.0 and 4.0 mg/kg).