Ginsenoside Ra1
(Synonyms: 人参皂苷 Ra1) 目录号 : GC36138
Ginsenoside Ra1 是人参中的成分，抑制缺氧/复氧诱导的蛋白酪氨酸激酶 (PTK) 的激活。
Cas No.:83459-41-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Ginsenoside Ra1 is a component from ginseng, inhibits protein tyrosine kinase (PTK) activation induced by hypoxia/reoxygenation[1].
[1]. Dou DQ, et al. The inhibitory effects of ginsenosides on protein tyrosine kinase activated by hypoxia/reoxygenation in cultured human umbilical vein endothelial cells. Planta Med. 2001 Feb;67(1):19-23.
| Cas No. | 83459-41-0 | SDF | |
| 别名 | 人参皂苷 Ra1 | ||
| 分子式 | C58H98O26 | 分子量 | 1211.38 |
| 溶解度 | DMSO : 100 mg/mL (82.55 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.8255 mL | 4.1275 mL | 8.255 mL |
| 5 mM | 0.1651 mL | 0.8255 mL | 1.651 mL |
| 10 mM | 0.0826 mL | 0.4128 mL | 0.8255 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Cloning and characterization of ginsenoside Ra1-hydrolyzing beta-D-xylosidase from Bifidobacterium breve K-110
J Microbiol Biotechnol 2012 Apr;22(4):535-40.PMID:22534302DOI:10.4014/jmb.1110.10001.
beta-D-Xylosidase (E.C. 3.2.1.37) from Bifidobacterium breve K-110, which hydrolyzes Ginsenoside Ra1 to ginsenoside Rb2, was cloned and expressed in Escherichia coli. The (His6)-tagged recombinant enzyme, designated as XlyBK- 110, was efficiently purified using Ni²⁺-affinity chromatography (109.9-fold, 84% yield). The molecular mass of XylBK- 100 was found to be 55.7 kDa by SDS-PAGE. Its sequence revealed a 1,347 bp open reading frame (ORF) encoding a protein containing 448 amino acids, which showed 82% identity (DNA) to the previously reported glycosyl hydrolase family 30 of Bifidobacterium adolescentis ATCC 15703. The Km and Vmax values toward p-nitrophenyl-beta-D-xylopyranoside (pNPX) were 1.45mM and 10.75 micromol/min/mg, respectively. This enzyme had pH and temperature optima at 6.0 and 45 degrees C, respectively. XylBK-110 acted to the greatest extent on xyloglucosyl kakkalide, followed by pNPX and Ginsenoside Ra1, but did not act on p-nitrophenyl-alpha-Larabinofuranoside, p-nitrophenyl-beta-D-glucopyranoside, or p-nitrophenyl-beta-D-fucopyranoside. In conclusion, this is the first report on the cloning and expression of beta-Dxylosidase- hydrolyzing Ginsenoside Ra1 and kakkalide from human intestinal microflora.
Purification and characterization of ginsenoside Ra-hydrolyzing beta-D-xylosidase from Bifidobacterium breve K-110, a human intestinal anaerobic bacterium
Biol Pharm Bull 2003 Aug;26(8):1170-3.PMID:12913270DOI:10.1248/bpb.26.1170.
Beta-D-Xylosidase (EC 3.2.1.37) has been purified from ginsenoside Ra-metabolizing Bifidobacterium breve K-110, which was isolated from human intestinal microflora. beta-D-Xylosidase was purified to apparent homogeneity by a combination of ammonium sulfate precipitation, QAE-cellulose, butyl-toyopearl, hydroxyapatit and Q-Sepharose column chromatographies with the final specific activity of 51.8 micromol/min/mg. Molecular weight of beta-D-xylosidase is 49 kDa by SDS-PAGE and gel filtration, which consisted of a single subunit. beta-D-Xylosidase showed optimal activity at pH 5.0 and 37 degrees C. The purified enzyme was potently inhibited by PCMS. beta-D-Xylosidase acted to the greatest extent on p-nitrophenyl-beta-D-xylopyranoside, followed by Ginsenoside Ra1 and ginsenoside Ra2. This enzyme hydrolyzed xylan to xylose, but did not act on p-nitrophenyl-beta-glucopyranoside, p-nitrophenyl-beta-galactopyranoside or p-nitrophenyl-beta-D-fucopyranoside. These findings suggest that this is the first reported purification of ginsenoside-hydrolyzing beta-D-xylosidase from an anaerobic Bifidobacterium sp.
[Chemical constituents from roots and rhizomes of Panax ginseng cultivated in Jilin province]
Zhongguo Zhong Yao Za Zhi 2013 Sep;38(17):2807-17.PMID:24380303doi
The chemical constituents of the roots and rhizomes of Panax ginseng were systematically investigated by various column chromatographic methods including Amberlite XAD-4 macroporous adsorptive resins and silica gel as well as high-performance liquid chromatography, and their chemical structures were identified by physico-chemical properties and spectral analyses. Twenty-eight compounds were isolated from the 70% ethanolic-aqueous extract and identified as koryoginsenoside R1 (1), ginsenoside Rg1 (2), ginsenoside Rf (3), notoginsenoside R2 (4), ginsenoside Rg2 (5), notoginsenoside Fe (6), ginsenjilinol (7), ginsenoside Re5 (8), noto-ginsenoside N (9), notoginsenoside R1 (10), ginsenoside Re2 (11), ginsenoside Re1 (12), ginsenoside Re (13), ginsenoside Rs2 (14), ginsenoside Ro methyl ester (15), ginsenoside Rd (16), ginsenoside Re3 (17), ginsenoside Re4 (18), 20-gluco-ginsenoside Rf (19), ginsenoside Ro (20), ginsenoside Rc (21), quinquenoside-R1 (22), ginsenoside Ra2 (23), ginsenoside Rb1 (24), Ginsenoside Ra1 (25), ginsenoside Ra3 (26), ginsenoside Rb2 (27), and notoginsenoside R4 (28). All isolated compounds are 20 (S) -protopanaxadiol or protopanaxatriol type triterpenoid saponins. Compound 1 was isolated from the roots and rhizomes of P. ginseng cultivated in Jilin province for the first time and compound 6 was isolated from the roots and rhizomes of P. ginseng for the first time. The 1H-NMR data of compounds 6, 14 and 19 were assigned for the first time.
Systematic exploration of Astragalus membranaceus and Panax ginseng as immune regulators: Insights from the comparative biological and computational analysis
Phytomedicine 2021 Jun;86:153077.PMID:31477352DOI:10.1016/j.phymed.2019.153077.
Background: Immune system plays a decisive role for defending various pathogenic microorganisms. Astragalus membranaceus (AM) and Panax ginseng (PG) are two tonic herbs used in traditional Chinese medicine (TCM) as immune booster and help to control diseases with their healthy synergistic effect on immune system. Purpose: This study was aimed to investigate the promote effect and molecular mechanisms of AM and PG on immune system as booster and to control the target diseases using animal and computational systematic study. Methods: Computational models including absorption, distribution, metabolism, and elimination (ADME) with weighted ensemble similarity (WES) algorithm-based models and ClueGo network analysis were used to find the potential bioactive compounds targets and pathways, which were responsible for immune regulation. Viscera index analysis, proliferation activity of splenic lymphocytes and cytotoxic activity of NK cells assays were performed to validate the effect of AM and PG on immune system of long-term administrated mice. Metabonomic study of mice plasma was conducted to investigate effect of AM and PG on the endogenous metabolic perturbations, together with correlation analysis. Results: AM and PG simultaneously showed the ability to strengthen the immune system function including enhancement of spleen and thymus index, proliferation of splenic lymphocytes and cytotoxic activity of NK cells. Besides, the different molecular mechanisms of AM and PG on immune regulation were also investigated by analyzing the potential bioactive compounds, enzymes actions and pathways. Quercetin, formononetin and kaempferol were the main immune-related compounds in AM, while Ginsenoside Ra1, ginsenoside Rh1 and kaempferol in PG. About 10 target proteins were found close to immune regulation, including acetylcholinesterase (ACHE, common target in AM and PG), sphingosine kinase 1(SPHK1), cytidine deaminase (CDA), and Choline O-acetyltransferase (CHAT). Glycerophospholipid metabolism was regulated in both AM and PG groups. Pyrimidine metabolism and sphingolipid metabolism were considered as the special pathway in AM groups. Energy metabolism and glycerolipid metabolism were the special pathways in PG groups. Conclusion: A novel comprehensive molecular mechanism analysis method was established and applied to clarify the scientific connotation of AM and PG as immune regulation, with similar herbal tonic effect provided in clinical practice of TCM, which can provide a new line of research for drug development (immune booster) using AM and PG.
Systematic analysis of the material basis and mechanism of total saponins of mountain cultivated ginseng against doxorubicin-induced cardiotoxicity based on integrating network pharmacology and in vivo substance profiling
Phytochem Anal 2022 Dec 18.PMID:36529443DOI:10.1002/pca.3194.
Introduction: Doxorubicin-induced cardiotoxicity (DIC) is a serious obstacle to oncologic treatment. Mountain cultivated ginseng (MCG) exhibits stronger pharmacological effects than cultivated ginseng (CG) mainly due to the differences in ginsenosides. However, the material basis and the underlying mechanism of the protective effects of total saponins of MCG (TSMCG) against DIC are unclear. Objectives: We aimed to elucidate the material basis and the pharmacodynamic effects of TSMCG on DIC as well as the underlying mechanisms. Methods: To comprehensively analyze the effective substances, the chemical components of TSMCG and their prototypes or metabolites in vivo were characterized through UHPLC/Q-TOF-MS. Then, an absorbed component-target-disease network was established to explore the mechanisms underlying the protective effects of TSMCG against DIC. H9c2 cells were employed for pharmacodynamic assays. The mechanism was verified by Western blot and molecular docking simulations. Results: A total of 56 main ginsenosides were identified in TSMCG, including 27 ginsenosides of PPD type, 15 ginsenosides of PPT type, two ginsenosides of OA types, and 12 ginsenosides of other types. Moreover, 55 ginsenoside prototypes or metabolites in vivo were tentatively characterized. Ginsenoside Ra1 , a differential compound between MCG and CG, could be metabolized by oxidation and deglycosylation. Network pharmacology showed that AKT1, p53, and STAT3 are core targets of 62 intersecting genes. Molecular docking results indicated that most of the ginsenosides have favorable affinity with these core targets. After doxorubicin exposure, TSMCG could increase cell viability and inhibit apoptosis in a dose-dependent manner. Conclusion: Our work reveals a novel comprehensive strategy to study the material basis of the protective effects of TSMCG against DIC and the underlying mechanisms through integrating in vivo substance identification, metabolic profiling, network pharmacology, pharmacodynamic evaluation, and mechanism verification.