Ginsenoside Rk3
(Synonyms: 人参皂甙 Rk3) 目录号 : GC31817
GinsenosideRk3存在于Panaxnotoginseng的根中。在HepG2细胞中GinsenosideRk3抑制TNF-α诱导的NF-κB转录活性，IC50值为14.24±1.30μM。
Cas No.:364779-15-7
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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Cell experiment: |
HepG2 and SK-Hep1 cells are maintained in Dulbecco’s modified Eagle’s medium containing 10% heat-inactivated fetal bovine serum, 100 units/mL Penicillin, and 10 μg/mL Streptomycin, at 37°C and 5% CO2. Cell-Counting Kit (CCK)-8 is used to analyze the effect of compounds (e.g., Ginsenoside Rk3; 0.01, 0.1, 1 and 10 uM) on cell toxicity. Cells are cultured overnight in 96-well plate (~1×104 cells/well). Cell toxicity is assessed after the addition of compounds on dose-dependent manner. After 24 h of treatment, 10 μL of the CCK-8 solution is added to triplicate wells, and incubated for 1 h. Absorbance is measured at 450 nm to determine viable cell numbers in wells[1]. |
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Animal experiment: |
Mice[2]Four- to 5-week-old male nude mice are selected and housed under aseptic conditions. The animals are exposed to a phase shift of the light/dark cycle for one week and allowed free access to a normal diet. All animal handling is performed under a laminar flow hood. The H460 xenograft model is established. Cell suspensions at a density of 4-5×106 cells are subcutaneously implanted into the left axilla of each mouse. Tumor engraftment is considered successful when the tumors are clearly visible, which occurs after one to two weeks. The tumor-bearing mice are randomly divided into the following 5 groups (5 mice per group) according to tumor size and body weight: control group (0.9% saline solution), Ginsenoside Rk3-treated group (5/10/20 mg/kg), and Gefitinib-treated group (20 mg/kg). The indicated doses (5-20 mg/kg) of Ginsenoside Rk3 are safe for mice as determined by preliminary acute oral toxicity tests. The dose of Gefitinib is based on the results from another study. Mice are intragastrically treated daily for 21 days. The tumor volumes are estimated. The body weights and tumor volumes of the mice in each group are measured twice per week. After 21 days, all animals are euthanized, and all tumor tissues are removed, weighed, and collected. |
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References: [1]. Cho K, et al. Inhibition of TNF-α-Mediated NF-κB Transcriptional Activity by Dammarane-Type Ginsenosidesfrom Steamed Flower Buds of Panax ginseng in HepG2 and SK-Hep1 Cells. Biomol Ther (Seoul). 2014 Jan;22(1):55-61. |
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Ginsenoside Rk3 is present in the roots Panax notoginseng herbs. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC50 of 14.24±1.30 μM in HepG2 cells.
Ginsenoside Rk3 exerts the strong activity inhibiting NF-κB in a dose-dependent manner. HepG2 cells are pre-treated with different ginsenosides at concentrations ranging from 0.01 to 10 μM for 1 h, and induced with TNF-α for 20 h. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC50 of 14.24±1.30 μM. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC50 of 15.32±0.29 μM in SK-Hep1 cells, consistent with the data from HepG2 cells. Consistent with the inhibition of NF-κB, Ginsenoside Rk3 inhibits the induction of IL8, CXCL1, iNOS, and ICAM1 mRNA significantly in a dose-dependent manner[1].
The inhibitory effects of Ginsenoside Rk3 (Rk3) on tumor progression are studied in vivo using a H460 xenograft model in nude mice. Compared with the control group, a significant inhibition of tumor growth (volume) is observed in the Ginsenoside Rk3-treated group. Twenty-one days after treatment initiation, tumor growth is significantly inhibited by approximately 62.99% in the mice receiving 20 mg/kg Ginsenoside Rk3, similar to the inhibitory effect observed in the 20 mg/kg Gefitinib-treated group (57.21%). Compared with the control group, tumor growth is moderately inhibited in the mice receiving 10 and 5 mg/kg Ginsenoside Rk3, with inhibition rates of 32.54% and 11.84%, respectively[2].
[1]. Cho K, et al. Inhibition of TNF-α-Mediated NF-κB Transcriptional Activity by Dammarane-Type Ginsenosidesfrom Steamed Flower Buds of Panax ginseng in HepG2 and SK-Hep1 Cells. Biomol Ther (Seoul). 2014 Jan;22(1):55-61. [2]. Duan Z, et al. Anticancer effects of ginsenoside Rk3 on non-small cell lung cancer cells: in vitro and in vivo. Food Funct. 2017 Oct 18;8(10):3723-3736.
| Cas No. | 364779-15-7 | SDF | |
| 别名 | 人参皂甙 Rk3 | ||
| Canonical SMILES | C[C@@]([C@@]12C)(C[C@H](O[C@]([C@@H]([C@@H](O)[C@@H]3O)O)([H])O[C@@H]3CO)[C@@]4([H])C5(C)C)[C@@](C[C@@H](O)[C@]1([H])[C@@H](C(CC/C=C(C)/C)=C)CC2)([H])[C@]4(CC[C@@H]5O)C | ||
| 分子式 | C36H60O8 | 分子量 | 620.86 |
| 溶解度 | DMSO : 100 mg/mL (161.07 mM; Need ultrasonic) | 储存条件 | 4°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 | 1.6107 mL | 8.0533 mL | 16.1067 mL |
| 5 mM | 0.3221 mL | 1.6107 mL | 3.2213 mL |
| 10 mM | 0.1611 mL | 0.8053 mL | 1.6107 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 Rk3 ameliorates high-fat-diet/streptozocin induced type 2 diabetes mellitus in mice via the AMPK/Akt signaling pathway
Ginsenoside Rk3 (G-Rk3) is a main active ingredient of ginsenosides. Several recent studies demonstrated that ginsenosides have potential anti-type 2 diabetes mellitus (T2DM) properties. To evaluate the anti-T2DM effect of G-Rk3 and verify its potential mechanism, a high-fat-diet/streptozocin (HFD/STZ) induced model of T2DM in C57BL/6 mice and a high glucose induced insulin resistance model of HepG2 cells were applied in this research. Our analysis indicated that G-Rk3 reduced HFD/STZ induced hyperglycemia, and serum insulin and inflammation levels, and ameliorated glucose tolerance and insulin resistance, and prevented liver histological changes. Furthermore, it also significantly reduced lipid accumulation as shown by lower TG, LDL-C and TC serum concentrations and Oil Red O staining in liver tissues. The hypoglycemic effect of G-Rk3 seemed to be partially mediated via the inhibition of hepatic gluconeogenesis, which was supported by the activated p-Akt, p-FoxO1 and GLUT2 and inhibited FoxO1, PEPCK and G6pase protein expressions in the liver as well as increased glucose uptake in high glucose induced HepG2 cells. The gene expressions of hepatic gluconeogenesis were also down-regulated by G-Rk3 in HFD/STZ induced T2DM mice. In addition, G-Rk3 suppressed HFD/STZ induced lipid accumulation by regulating related gene and protein expressions such as p-ACC, FAS and SREBP-1, which are the downstream targets of AMPK. AMPK and Akt inhibitors significantly reversed G-Rk3 mediated hepatic gluconeogenesis and lipid accumulation. Thus, our study is the first to illustrate that G-Rk3 mediates hepatic gluconeogenesis and lipid accumulation via activating the AMPK/Akt signaling pathway in HFD/STZ induced T2DM mice.
Ginsenoside Rk3 alleviates gut microbiota dysbiosis and colonic inflammation in antibiotic-treated mice
Ginsenoside Rk3 is a natural prebiotic found in ginseng, has excellent pharmacological efficacy, especially antitumor effects, and can greatly benefit human health. Here, we investigated the impact of Rk3 intake on modulation of the gut microbiota and their metabolites as well as its effect on low-grade inflammation in mice. C57BL/6JFandd mice were administered different doses of Rk3 for two weeks after establishment of an antibiotic-mediated gut microbiota disturbance model. Interestingly, Rk3 intake induced substantial changes in the gut microbiota composition, enriched the Bacteroides, Alloprevotella and Blautia genera, and effectively ameliorated gut microbiota dysbiosis, with significantly decreased Firmicutes/Bacteroidetes ratios. These changes were accompanied by beneficial alterations in gut microbiota diversity and improved short-chain fatty acid levels. In addition, we found that Rk3 intervention repaired intestinal barrier dysfunction by increasing the expression of tight junction proteins (ZO-1, Occludin and Claudin-1), reducing colonic inflammatory cytokine levels, and suppressing TNF-α, IL-1β, and IL-6 overproduction. In conclusion, Rk3 improves intestinal inflammation and induces potentially beneficial changes in the gut microbiota, and these findings help elucidate host-microbe interactions.
Ginsenoside Rk3 Suppresses Hepatocellular Carcinoma Development through Targeting the Gut-Liver Axis
Hepatocellular carcinoma (HCC) is the third leading cause of cancer death worldwide. Our previous reports showed that ginsenoside Rk3 provided excellent efficacy in alleviating the intestinal inflammatory response and protecting the liver, but its mechanism for HCC prevention remains to be explored. Here, the results suggested that Rk3 displayed potent antitumor effects against a dimethyl nitrosamine- and CCl4-induced HCC mouse model. Results revealed that Rk3 application inhibited liver injury, fibrosis, and cirrhosis. In parallel, Rk3 lowered the inflammatory response by decreasing the expression of inflammatory cytokines, inducing apoptosis, and blocking the cell cycle. Meanwhile, Rk3 effectively ameliorated the gut microbiota dysbiosis. Furthermore, correlation analysis revealed that the LPS-TLR4 signaling pathway, which was inhibited by Rk3, plays a key role in preventing HCC. To conclude, our research provides valuable insights into how Rk3 application targets the gut-liver axis and suppresses HCC development, suggesting that Rk3 might be a promising candidate for clinical treatment of HCC.
Ginsenoside Rk3 Inhibits the Extramedullary Infiltration of Acute Monocytic Leukemia Cell via miR-3677-5p/CXCL12 Axis
Background: Acute monocytic leukemia belongs to type M5 of acute myeloid leukemia (AML) classified by FAB, which appears a high incidence of extramedullary infiltration (EMI) and poor prognosis. In this study, we observed the inhibitory effect of ginsenoside Rk3 on the EMI of monocytic leukemia cells and initially explored its related mechanism of targeting the miR-3677-5p/CXCL12 axis.
Methods: The MTT assay and colony formation assay were used to detect the inhibitory effect of Rk3 on proliferation. Both cellular migration and invasion were observed by the Transwell assay. The expression levels of miR-3677-5p, CXCL12, and CXCR4 were detected by RT-qPCR and Western blot, as well as overexpression of miR-3677-5p by transfected with lentivirus and detection of a dual luciferase reporter gene. The expression of MMP2 and TIMP2 was detected by immunofluorescence.
Results: Rk3 effectively inhibits the proliferation, migration, and invasion associated with EMI of leukemia. The leukemia cells of M5 patients with EMI showed low expression of miR-3677-5p but high expression of the mRNA of CXCL12 and CXCR4. Overexpression of miR-3677-5p or intervention of CXCL12 effectively inhibited the proliferation, migration, and invasion of SHI-1 cells. The luciferase assay showed that CXCL12 was the downstream target gene of miR-3677-5p. After overexpression of miR-3677-5p or intervention of CXCL12 in combination with Rk3, the inhibitory effect on the proliferation, migration, and invasion of SHI-1 cells was more obvious. Importantly, Rk3 significantly regulated the expression levels of miR-3677-5p, CXCL12, CXCR4, and EMI-related functional proteins including MMP2 and TIMP2. Overexpression of miR-3677-5p or intervention of CXCL12 also regulated the expression of MMP2 and TIMP2.
Conclusions: The leukemia cells of M5 patients with EMI appeared to have low expression of miR-3677-5p and high expression of the mRNA of CXCL12 and CXCR4, which may be used as indicators of EMI and poor prognosis. Rk3 is effective in inhibiting the EMI of SHI-1 cells by targeting the miR-3677-5p/CXCL12 axis.
Ginsenoside Rk3 Ameliorates Obesity-Induced Colitis by Regulating of Intestinal Flora and the TLR4/NF-κB Signaling Pathway in C57BL/6 Mice
Obesity-induced colonic inflammation-stimulated colitis is one of the main causes of colorectal cancer. Dietary phytochemicals are considered to be an effective strategy for relieving obesity-induced inflammatory diseases such as diabetes and colitis. Ginsenoside Rk3 (Rk3) is the main bioactive component of ginseng. Our previous study has demonstrated that Rk3 can effectively alleviate obesity-induced type 2 diabetes, but whether it plays a beneficial role in obesity-induced colitis remains poorly understood. Here, we found that Rk3 intervention repaired the intestinal barrier dysfunction by increasing the expression of the tight junction proteins (zonula occludens-1, claudin, and occludin), and reduced colonic inflammatory cytokine levels, oxidative stress, and macrophage infiltration in high-fat diet-induced mice. Importantly, Rk3 effectively ameliorated the metabolic dysbiosis of intestinal flora with significantly decreased Firmicute/Bacteroidete ratios and suppressed the inflammatory cascade by inhibiting the TLR4/NF-κB signaling pathway. Taken together, our findings indicate that Rk3 can be used as a potential natural anti-inflammatory agent to reduce chronic obesity-induced colitis.