Ginsenoside Rg5
(Synonyms: 人参皂甙 Rg5) 目录号 : GC31706
A ginsenoside with diverse biological activities
Cas No.:186763-78-0
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
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Kinase experiment: |
HUVECs are cultured in 24-well plates overnight. The cells are changed to serum-free M199 and incubated for 1 h. The medium is removed, and cells are incubated with fresh serum-free medium containing 0.1 μM-50 mM Ginsenoside Rg5 at 37°C for 20 min followed by the addition of 50 μL (1 μCi) of [125I]IGF-1 and then further incubated for 10 min. The medium is decanted, and cell plates are washed twice with serum-free medium. Cells are lysed in 300 μL of 0.1 N NaOH solution containing 0.1% SDS, transferred to scintillation vials, and mixed with 1 mL of Ultima Gold mixture solution. Cell-associated [125I]IGF-1 is analyzed in a scintillation counter. The nonspecific binding is determined by coincubation with unlabeled IGF-1 (50 nM)[1]. |
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Cell experiment: |
MCF-7 (HER2-/ER+) and MDA-MB-453 (HER2+/ER-) human breast cancer cell lines are maintained using RPMI 1640 medium supplemented with 10% (vol/vol) FBS plus 100 units/mL Penicillin and Streptomycin in a 5% carbon dioxide air incubator at 37°C. Cell cytotoxicity is measured by MTT assay. Cells are seeded in 96-well tissue culture plates at the density of 0.2×104 cells per well with 100 μL medium, and are allowed to become attached for 24 h. One hundred microliters of the medium with different concentrations of Ginsenoside Rg5 (e.g., 0 μM, 25 μM, 50 μM, and 100 μM) are added to each well. At indicated times, 30 μL MTT stock solution (3 mg/mL) are added to each well. After culturing the cells at 37°C for 2 h, DMSO is added to dissolve the formazan crystals. The absorbance is read at the wavelength of 540 nm with a microplate reader[3]. |
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Animal experiment: |
Mice[2]Male ICR mice (6 to 8 weeks old), weighing 25-27 g, are used. After acclimation for one week, mice are randomly assigned into 4 experimental groups with 8 mice in each group: normal control, Cisplatin control, and Cisplatin+Ginsenoside Rg5 groups (10 and 20 mg/kg, respectively). Ginsenoside Rg5 is administered intragastrically at the dose of 10 and 20 mg/kg for 10 days. On the 7th day, animals in Cisplatin control and Ginsenoside Rg5-treated groups receive a single intraperitoneal injection of Cisplatin (25 mg/kg) to induce nephrotoxicity in mice. Mice are anaesthetized with pentobarbital, subsequently sacrificed at 72 h after Cisplatin injection (Day 10). Blood samples are collected and then centrifuged at 3000 rpm to separate the serum and stored at -20 °C for determining blood urea nitrogen (BUN) and creatinine (CRE) levels. |
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References: [1]. Cho YL, et al. Specific activation of insulin-like growth factor-1 receptor by ginsenoside Rg5 promotes angiogenesis and vasorelaxation. J Biol Chem. 2015 Jan 2;290(1):467-77. |
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Ginsenoside Rg5 is a ginsenoside originally isolated from P. ginseng that has diverse biological activities, including anticancer, anti-inflammatory, neuroprotective, and antioxidant properties.1,2,3 It inhibits the growth of HeLa and MS751 cervical cancer cells (IC50s = ~2.5-10 μM) and induces apoptosis in a concentration-dependent manner.1 Ginsenoside Rg5 (5 and 10 μM) inhibits LPS-induced increases in IL-1β, TNF-α, COX-2, and inducible nitric oxide synthase (iNOS) protein levels in murine alveolar macrophages.2 It also inhibits LPS-induced increases in the number of neutrophils and protein levels of IL-1β, TNF-α, COX-2, and iNOS in lung in a mouse model of acute lung inflammation when administered at a dose of 10 mg/kg. In a rat model of Alzheimer's disease induced by streptozotocin , ginsenoside Rg5 blocks STZ-induced increases in amyloid-β accumulation in the hippocampus and cerebral cortex and prevents STZ-induced decreases in step through latency time in a passive avoidance foot-shock test in a dose-dependent manner.3
1.Liang, L.-D., He, T., Du, T.-W., et al.Ginsenoside?Rg5 induces apoptosis and DNA damage in human cervical cancer cellsMol. Med. Rep.11(2)940-946(2015) 2.Kim, T.-W., Joh, E.-H., Kim, B., et al.Ginsenoside Rg5 ameliorates lung inflammation in mice by inhibiting the binding of LPS to toll-like receptor-4 on macrophagesInt. Immunopharmacol.12(1)110-116(2012) 3.Chu, S., Gu, J., Feng, L., et al.Ginsenoside Rg5 improves cognitive dysfunction and beta-amyloid deposition in STZ-induced memory impaired rats via attenuating neuroinflammatory responsesInt. Immunopharmacol.19(2)317-326(2014)
| Cas No. | 186763-78-0 | SDF | |
| 别名 | 人参皂甙 Rg5 | ||
| Canonical SMILES | C[C@@]([C@@]12C)(CC[C@@]3([H])C4(C)C)[C@@](C[C@@H](O)[C@]1([H])[C@@H](/C(C)=C/C/C=C(C)\C)CC2)([H])[C@]3(CC[C@@H]4O[C@@](O[C@H](CO)[C@@H](O)[C@@H]5O)([H])[C@@H]5O[C@]([C@@H]([C@@H](O)[C@@H]6O)O)([H])O[C@@H]6CO)C | ||
| 分子式 | C42H70O12 | 分子量 | 767 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 10 mg/ml | 储存条件 | Store at -20°C,protect from light |
| 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 | 1.3038 mL | 6.5189 mL | 13.0378 mL |
| 5 mM | 0.2608 mL | 1.3038 mL | 2.6076 mL |
| 10 mM | 0.1304 mL | 0.6519 mL | 1.3038 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。
Ginsenoside Rg5: A Review of Anticancer and Neuroprotection with Network Pharmacology Approach
Ginsenoside Rg5 (G-Rg5) is a rare ginsenoside isolated from ginseng (Panax ginseng C.A. Meyer), and this compound is increasingly known for its potent pharmacological activities. This study aimed to provide a comprehensive review of the main activities and mechanisms of G-Rg5 by adopting network pharmacological analysis combined with a summary of published articles. The 100 target genes of G-Rg5 were searched through available database, subjected to protein-protein interaction (PPI) network generation and then core screening. The results showed that G-Rg5 has promising anticancer and neuroprotective effects. By summarizing these two pharmacological activities, we found that G-Rg5 exerts its therapeutic effects mainly through PI3K/AKT, MAPK signaling pathways, and the regulation of apoptosis and cell cycle. And these results were corroborated by KEGG analysis. Likewise, molecular docking of the related proteins was performed, and the binding energies were all less than [Formula: see text]7.0[Formula: see text]kJ/mol, indicating that these proteins had excellent binding capacity with G-Rg5. The network pharmacology results revealed many potential G-Rg5 mechanisms, which need to be further explored. We expect that the network pharmacology approach and molecular docking techniques can help us gain a deeper understanding of the therapeutic mechanisms of different ginsenosides and even the ginseng plant, for further developing their therapeutic potential as well as clinical applications.
Pharmacological activities of ginsenoside Rg5 (Review)
Ginseng, a perennial plant belonging to genus Panax, has been widely used in traditional herbal medicine in East Asia and North America. Ginsenosides are the most important pharmacological component of ginseng. Variabilities in attached positions, inner and outer residues and types of sugar moieties may be associated with the specific pharmacological activities of each ginsenoside. Ginsenoside Rg5 (Rg5) is a minor ginsenoside synthesized during ginseng steaming treatment that exhibits superior pharmaceutical activity compared with major ginsenosides. With high safety and various biological functions, Rg5 may act as a potential therapeutic candidate for diverse diseases. To date, there have been no systematic studies on the activity of Rg5. Therefore, in this review, all available literature was reviewed and discussed to facilitate further research on Rg5.
Ginsenoside Rg5 Inhibits Human Osteosarcoma Cell Proliferation and Induces Cell Apoptosis through PI3K/Akt/mTORC1-Related LC3 Autophagy Pathway
The function and mechanism underlying the suppression of human osteosarcoma cells by ginsenoside-Rg5 (Rg5) was investigated in the present study. MG-63, HOS, and U2OS cell proliferation was determined by MTT assay after Rg5 treatment for 24 h. Rg5 inhibited human osteosarcoma cell proliferation effectively in a dose-dependent manner. The range of effective inhibitory concentrations was 160-1280 nM. Annexin V-FITC and PI double-staining assay revealed that Rg5 induced human osteosarcoma cell apoptosis. Western blotting, qRT-PCR, and FACS experiments revealed that Rg5 inhibited human osteosarcoma cells via caspase-3 activity which was related to the LC3-mediated autophagy pathway. Rg5 decreased the phosphorylation of PI3K, Akt, and mTORC1 activation. In contrast, LC3-mediated autophagy and caspase-3 activity increased significantly. A PI3K/AKT stimulator, IGF-1, reversed Rg5-induced cell autophagy and apoptosis in MG-63 cells. Collectively, the current study demonstrated that Rg5 induced human osteosarcoma cell apoptosis through the LC3-mediated autophagy pathway. Under physiological conditions, activation of PI3K/AKT/mTORC1 inhibits LC3 activity and caspase-3-related cell apoptosis. However, Rg5 activated LC3 activity by inhibiting the activation of PI3K/AKT/mTORC1. The present study indicated that Rg5 could be a promising candidate as a chemotherapeutic agent against human osteosarcoma.
Ginsenoside Rg5 allosterically interacts with P2RY12 and ameliorates deep venous thrombosis by counteracting neutrophil NETosis and inflammatory response
Background: Deep venous thrombosis (DVT) highly occurs in patients with severe COVID-19 and probably accounted for their high mortality. DVT formation is a time-dependent inflammatory process in which NETosis plays an important role. However, whether ginsenoside Rg5 from species of Panax genus could alleviate DVT and its underlying mechanism has not been elucidated.
Methods: The interaction between Rg5 and P2RY12 was studied by molecular docking, molecular dynamics, surface plasmon resonance (SPR), and molecular biology assays. The preventive effect of Rg5 on DVT was evaluated in inferior vena cava stasis-induced mice, and immunocytochemistry, Western blot, and calcium flux assay were performed in neutrophils from bone marrow to explore the mechanism of Rg5 in NETosis via P2RY12.
Results: Rg5 allosterically interacted with P2RY12, formed stable complex, and antagonized its activity via residue E188 and R265. Rg5 ameliorated the formation of thrombus in DVT mice; accompanied by decreased release of Interleukin (IL)-6, IL-1β, and tumor necrosis factor-α in plasma; and suppressed neutrophil infiltration and neutrophil extracellular trap (NET) release. In lipopolysaccharide- and platelet-activating factor-induced neutrophils, Rg5 reduced inflammatory responses via inhibiting the activation of ERK/NF-κB signaling pathway while decreasing cellular Ca2+ concentration, thus reducing the activity and expression of peptidyl arginine deiminase 4 to prevent NETosis. The inhibitory effect on neutrophil activity was dependent on P2RY12.
Conclusions: Rg5 could attenuate experimental DVT by counteracting NETosis and inflammatory response in neutrophils via P2RY12, which may pave the road for its clinical application in the prevention of DVT-related disorders.
Ginsenoside Rg5 Improves Insulin Resistance and Mitochondrial Biogenesis of Liver via Regulation of the Sirt1/PGC-1α Signaling Pathway in db/db Mice
Type 2 diabetes mellitus (T2DM) is a common metabolic syndrome that decreases insulin sensitivity and mitochondrial biogenesis in the liver. Our previous study demonstrated that ginsenoside Rg5 (Rg5) could attenuate renal injury in diabetic mice but its underlying mechanism in mitochondrial biogenesis and insulin sensitivity remains poorly understood. In this study, we found that Rg5 intervention significantly inhibited blood glucose increases in db/db mice, improved liver function damage and hepatocyte apoptosis, and activated the IRS-1/phosphatidylinositol 3-kinase/AKT insulin metabolism signaling pathway. Rg5 treatment also increased the level of glycogen synthesis and activated sirtuin1 (Sirt1) to increase glucose uptake and insulin sensitivity in insulin-resistant HepG2 (IR-HepG2) cells. Rg5 intervention also effectively improved liver oxidative stress and inflammation in db/db mice and increased mitochondrial biogenesis caused by T2DM. Additionally, the Rg5 treatment increased the mitochondrial mass in IR-HepG2 cells and activated Sirt1 to regulate the Sirt1/PGC-1α/mitofusin-2 mitochondrial biosynthesis pathway. Our findings demonstrated that Rg5 enhanced liver mitochondrial biogenesis and insulin sensitivity in db/db mice by activating the Sirt1/PGC-1α signaling pathway, suggesting the potential of Rg5 as a natural product for T2DM interventions.