Platycodin D3
(Synonyms: 桔梗皂苷 D3) 目录号 : GC36937
Platycodin D3 是桔梗中的三萜皂苷类化合物，具有抗 HCV 活性。
Cas No.:67884-03-1
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
Platycodin D3 is a triterpenoid saponin isolated from Platycodon grandiflorum, with anti-HCV activity[1]. HCV[1]
[1]. Kim JW, et al. Triterpenoid Saponins Isolated from Platycodon grandiflorum Inhibit Hepatitis C Virus Replication. Evid Based Complement Alternat Med. 2013;2013:560417.
| Cas No. | 67884-03-1 | SDF | |
| 别名 | 桔梗皂苷 D3 | ||
| Canonical SMILES | OC(C(C(OC1C(C(C(O)CO1)OC2C(C(CO)(O)CO2)O)O)C(C)O3)O)C3OC(C(C(O)CO4)O)C4OC(C56C(CC(C)(C)CC6)C7=CCC(C8(C(C(CO)(C(OC9OC(C(O)C(O)C9O)COC%10OC(C(O)C(O)C%10O)CO)C(O)C8)CO)CC%11)C)C%11(C)C7(C)CC5O)=O | ||
| 分子式 | C63H102O33 | 分子量 | 1387.46 |
| 溶解度 | DMSO : 100 mg/mL (72.07 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 | 0.7207 mL | 3.6037 mL | 7.2074 mL |
| 5 mM | 0.1441 mL | 0.7207 mL | 1.4415 mL |
| 10 mM | 0.0721 mL | 0.3604 mL | 0.7207 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。
Biocatalysis of Platycoside E and Platycodin D3 Using Fungal Extracellular β-Glucosidase Responsible for Rapid Platycodin D Production
Int J Mol Sci 2018 Sep 8;19(9):2671.PMID:30205574DOI:10.3390/ijms19092671.
Platycodi radix (i.e., Platycodon grandiflorum root) products (e.g., tea, cosmetics, and herbal supplements) are popular in East Asian nutraceutical markets due to their reported health benefits and positive consumer perceptions. Platycosides are the key drivers of Platycodi radixes' biofunctional effects; their nutraceutical and pharmaceutical activities are primarily related to the number and varieties of sugar side-chains. Among the various platycosides, platycodin D is a major saponin that demonstrates various nutraceutical activities. Therefore, the development of a novel technology to increase the total platycodin D content in Platycodi radix extract is important, not only for consumers' health benefits but also producers' commercial applications and manufacturing cost reduction. It has been reported that hydrolysis of platycoside sugar moieties significantly modifies the compound's biofunctionality. Platycodi radix extract naturally contains two major platycodin D precursors (platycoside E and Platycodin D3) which can be enzymatically converted to platycodin D via β-d-glucosidase hydrolysis. Despite evidence that platycodin D precursors can be changed to platycodin D in the Platycodi radix plant, there is little research on increasing platycodin D concentrations during processing. In this work, platycodin D levels in Platycodi radix extracts were significantly increased via extracellular Aspergillus usamii β-d-glucosidase (n = 3, p < 0.001). To increase the extracellular β-d-glucosidase activity, A. usamii was cultivated in a culture media containing cellobiose as its major carbon source. The optimal pH and temperature of the fungal β-d-glucosidase were 6.0 and 40.0 °C, respectively. Extracellular A. usamii β-d-glucosidase successfully converted more than 99.9% (w/v, n = 3, p < 0.001) of platycoside E and Platycodin D3 into platycodin D within 2 h under optimal conditions. The maximum level of platycodin D was 0.4 mM. Following the biotransformation process, the platycodin D was recovered using preparatory High Performance Liquid Chromatography (HPLC) and applied to in vitro assays to evaluate its quality. Platycodin D separated from the Platycodi radix immediately following the bioconversion process showed significant anti-inflammatory effects from the Lipopolysaccharide (LPS)-induced macrophage inflammatory responses with decreased nitrite and IL-6 production (n = 3, p < 0.001). Taken together, these results provide evidence that biocatalysis of Platycodi radix extracts with A. usamii may be used as an efficient method of platycodin D-enriched extract production and novel Platycodi radix products may thereby be created.
Protective Effects of Platycodin D3 on Airway Remodeling and Inflammation via Modulating MAPK/NF- κ B Signaling Pathway in Asthma Mice
Evid Based Complement Alternat Med 2022 Aug 10;2022:1612829.PMID:35990822DOI:10.1155/2022/1612829.
Background: Asthma is a disease with airway hyperresponsive and airway inflammation. Platycodin D is a triterpenoid saponin extracted from Platycodon grandiflorus root, which has various pharmacological activities. The study mainly explored the effects of Platycodin D3 (PD3) in airway remodeling and inflammation of asthma. Methods: The ovalbumin (OVA)-induced asthma mice were given PD3 (20 mg/kg, 40 mg/kg, and 80 mg/kg) in different groups. The asthma mice administrated with dexamethasone (DXM) were enrolled as the positive control group, and the normal control mice and asthma model mice separately received the same volume of saline. Mouse airway lung dynamic compliance (Cdyn) and total airway resistance (RL) were measured by the EMKA animal lung function analysis system. The inflammation factor levels were estimated by ELISA. Histopathological changes were tested by HE and PAS staining. The protein and phosphorylation levels of NF-κBp65, p38, ERK1/2, and JNK1/2 were detected by Western blot. Results: In asthmatic mice, PD3 enhanced the airway Cdyn and decreased RL to improve the airway hyperreactivity and alleviated the pathological injury of lung tissues. In addition, PD3 could reduce the infiltration of inflammatory cells in BALF and suppress the levels of eotaxin, IL-4, IL-5, IL-13, IFN-γ, and IgE. Furthermore, PD3 treatment inhibited the phosphorylation of NF-κBp65, p38, ERK1/2, and JNK1/2 proteins in asthma mice. Conclusion: PD3 treatment alleviated the airway remodeling and inflammation in asthmatic mice, which might be related to downregulating the phosphorylated proteins in the MAPK/NF-κB signaling pathway.
Determination of platycodin D and Platycodin D3 in rat plasma using liquid chromatography-tandem mass spectrometry
ScientificWorldJournal 2014 Jan 30;2014:231293.PMID:24592150DOI:10.1155/2014/231293.
Platycodon grandiflorum has long been used as a traditional oriental medicine for respiratory disorder. Platycodin D (PD) is known as the main component isolated from the root of PG. A simple and rapid liquid chromatography-tandem mass spectrometry (LC-MS/MS) method has been developed and validated for the quantitation of PD in rat plasma. Quantitation was performed on a triple quadrupole mass spectrometer employing electrospray ionization and multiple reaction monitoring in positive ion mode. The total chromatographic run time was 4.0 min, and the calibration curves of PD were linear over the concentration range of 50-10,000 ng/mL in rat plasma. The coefficient of variation and relative error at five QC levels were 1.0 to 8.8% and 0.7 to 8.7%, respectively. After a single oral administration of 500 mg/kg and a single intravenous administration of 25 mg/kg of 3% PD extract (a PG extract including 3% of PD), platycodin D and Platycodin D3 were detected and pharmacokinetic parameters were estimated. The oral bioavailability of platycodin D and Platycodin D3 was 0.29% and 1.35% in rats at 500 mg/kg of 3% PD extract of PG, respectively. The present method can be applied to pharmacokinetic analysis of platycodins and platycosides of the PG.
Platycodon grandiflorum Triggers Antitumor Immunity by Restricting PD-1 Expression of CD8+ T Cells in Local Tumor Microenvironment
Front Pharmacol 2022 Apr 14;13:774440.PMID:35496272DOI:10.3389/fphar.2022.774440.
In the tumor microenvironment (TME), the activation of programmed death-1 (PD-1)-programmed death ligand-1 (PD-L1) pathway is one of the main signals of immune escape and tumor deterioration. Clinically, the application of monoclonal antibodies slows down the progression of various malignancies and prolongs the survival of patients effectively. However, these treatments result in serious immune-related adverse events (irAEs) owning to systemic immune activation. Therefore, to achieve long-term therapeutic effects and low side effects, it is necessary to find drugs inhibiting the local PD-1/PD-L1 signaling pathway of the TME. Here, we discovered that Platycodon grandiflorum (PG), a medicine and food homology herb, reduced the expression of PD-1 on the surface of CD8+ T cells to exert antitumor effects in non-small cell lung cancer (NSCLC). Firstly, by combining systems pharmacology strategies and clinical data analysis, we found that PG has the potential to immunomodulate T cells and suppress tumors. Secondly, in vivo and in vitro experiments have confirmed the antitumor effect of the combination of Platycodin D and Platycodin D3, which is preferred and representative of the compounds. Mechanistically, PG increased the infiltration and killing activity of CD8+ T cells, which was related to the decrease of PD-1+ CD8+ T cells. Furthermore, we confirmed that PG regulated the expression of PD-1 on the surface of CD8+ T cells via reducing the secretion of VEGF-A regulated by the level of P-STAT3 in tumor cells. Additionally, PG also positively impacted the biological processes downstream of STAT3. Overall, we demonstrated that PG-mediated downregulation of PD-1 on the surface of CD8+ T cells represents a promising strategy to locally enhance T-cell responses and improve antitumor immunity.
Platycodin D and D3 increase airway mucin release in vivo and in vitro in rats and hamsters
Planta Med 2002 Mar;68(3):221-5.PMID:11914958DOI:10.1055/s-2002-23130.
The root of Platycodon grandiflorum has been widely used for the treatment of various chronic inflammatory diseases including airway disease in oriental medicine. The root extract of the plant has been known to be effective in the expectoration of sputum or mucus, thereby improving airway respiratory function and preventing secondary airway inflammation. In this study, we investigated the effect of platycodin D and D3, the saponin components that are anti-inflammatory components in Platycodon grandiflorum. Platycodin D and D3 increased mucin release from rat and hamster tracheal surface epithelial cell culture and also from intact rat trachea upon nebulization. The effect of Platycodin D3 was stronger than that of ATP, a potent mucin secretagogue and also of ambroxole, a mucolytic drug. The results from the present study suggest that platycodin D and D3 are useful as expectorant agents in the treatment of various airway diseases.