Polygalacin D
(Synonyms: 远志皂苷D) 目录号 : GC38545
Polygalacin D (PGD) 是从桔梗 Platycodon grandiflorum 中分离的具有抗癌和抗增殖特性的生物活性化合物。Polygalacin D 抑制 IAP 蛋白家族的表达，包括存活蛋白，cIAP-1 和 cIAP-2 蛋白，并通过抑制 GSK3β，Akt 的磷酸化和PI3K 的表达来阻断 PI3K/Akt 途径。Polygalacin D 通过 PI3K/Akt 途径诱导凋亡 (apoptosis)。
Cas No.:66663-91-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Polygalacin D (PGD) is a bioactive compound isolated from Platycodon grandiflorum (Jacq.) with anticancer and anti-proliferative properties.PGD suppresses the expression of the IAP family of proteins including survivin, cIAP-1 and cIAP-2 and blocks the PI3K/Akt pathway by inhibiting the phosphorylation of GSK3β, Akt and the expression of PI3K. Polygalacin D induces apoptosis[1]
Polygalacin D (0-40 µM; 48 hours) inhibits cell proliferation with IC50s of 26.49 µM in the A549 cells and 20.52 µM in the H460 cells[1].Polygalacin D (0-20 µM; 48 hours) increases the proportion of early and late apoptotic cells, and nuclear condensation is observed in A549 and H460 cells[1].Polygalacin D (0-20 µM; 48 hours) may exerts its apoptotic effects by regulating the apoptotic proteins and the IAP family of proteins in A549 and H460 cells[1]. Cell Proliferation Assay[1] Cell Line: A549 and H460 cancer cell lines
[1]. Seo YS, et al. Polygalacin D induces apoptosis and cell cycle arrest via the PI3K/Akt pathway in non-small cell lung cancer. Oncol Rep. 2018 Apr;39(4):1702-1710.
| Cas No. | 66663-91-0 | SDF | |
| 别名 | 远志皂苷D | ||
| 分子式 | C57H92O27 | 分子量 | 1209.32 |
| 溶解度 | Soluble in DMSO | 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 | 0.8269 mL | 4.1346 mL | 8.2691 mL |
| 5 mM | 0.1654 mL | 0.8269 mL | 1.6538 mL |
| 10 mM | 0.0827 mL | 0.4135 mL | 0.8269 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。
Polygalacin D suppresses esophageal squamous cell carcinoma growth and metastasis through regulating miR-142-5p/Nrf2 axis
Free Radic Biol Med 2021 Feb 20;164:58-75.PMID:33307164DOI:10.1016/j.freeradbiomed.2020.11.029.
Esophageal squamous cell carcinoma (ESCC) is a common malignancy worldwide with poor survival. High expression of nuclear factor erythroid 2-related factor 2 (Nrf2) is an antioxidant transcript factor that protects malignant cells from death. Polygalacin D (PGD), a bioactive compound isolated from Platycodongrandiflorum (Jacq.), has recently been reported to be an anti-tumor agent. This study aimed to investigate the anti-cancer effects of PGD and its underlying molecular mechanisms in human ESCC. Here, we confirmed that Nrf2 was over-expressed in clinical ESCC tissues and cell lines. PGD treatments markedly reduced Nrf2 expression in a dose- and time-dependent manner in ESCC cell lines. Importantly, we found that PGD significantly reduced proliferation, and induced G2/M cell cycle arrest and apoptosis in ESCC cells. Also, PGD dramatically triggered autophagy in ESCC cells, and autophagy inhibitor bafilomycinA1 (BafA1) greatly abrogated the inhibitory role of PGD in cell viability and apoptosis. In addition, PGD evidently provoked reactive oxygen species (ROS) accumulation in ESCC cells, and pre-treatment of ROS scavenger N-acetyl-l-cysteine (NAC) markedly abolished PGD-triggered cell death. PGD also dramatically repressed migration and invasion in ESCC cells. Mechanistic investigation revealed that Nrf2 gene was directly targeted by miR-142-5p. MiR-142-5p negatively regulated Nrf2 expression in ESCC cells. We notably found that PGD-inhibited proliferation, migration and invasion in ESCC were considerably rescued by miR-142-5p knockdown; however, ROS production, apoptosis and autophagy induced by PGD were almost eliminated when miR-142-5p was silenced. On the contrast, over-expressing miR-142-5p could remarkably promote the anti-ESCC effects of PGD. Experiments in vivo by the tumor xenograft model confirmed that miR-142-5p effectively improved the activity of PGD to repress tumor growth and lung metastasis. Both in vitro and in vivo studies showed that PGD had few side effects on normal cells and major organs. Collectively, our findings provided the first evidence that PGD could be an effective therapeutic strategy for ESCC treatment by regulating miR-142-5p/Nrf2 axis with few adverse effects.
Polygalacin D induces apoptosis and cell cycle arrest via the PI3K/Akt pathway in non-small cell lung cancer
Oncol Rep 2018 Apr;39(4):1702-1710.PMID:29393481DOI:10.3892/or.2018.6230.
Polygalacin D (PGD) is a bioactive compound isolated from Platycodon grandiflorum (Jacq.) and it has a similar structure to platycodin D, which is a well known anticancer agent. In the present study, we investigated the anti-proliferative effects of PGD using NSCLC cell lines. We evaluated the effects of PGD on proliferation, apoptosis and cell cycle arrest in A549 and H460 cells. PGD significantly induced apoptosis and nuclear condensation in both cell lines. Furthermore, PGD upregulated the cleavage of apoptotic proteins such as caspase-3, -9 and PARP. Additionally, treatment with PGD suppressed the expression of the IAP family of proteins including survivin, cIAP-1 and cIAP-2. Furthermore, PGD induced G0/G1-phase arrest in both cell lines. After treatment with PGD, the expression of TIMP-1, CDK2, cyclin A and cyclin E was reduced at the protein level. In addition, PGD blocked the PI3K/Akt pathway by inhibiting the phosphorylation of GSK3β, Akt and the expression of PI3K. Our results indicated that the anti-proliferative properties of PGD may result from the regulation of the PI3K/Akt pathway, which plays a critical role in cell survival and growth.
Conversion of Glycosylated Platycoside E to Deapiose-Xylosylated Platycodin D by Cytolase PCL5
Int J Mol Sci 2020 Feb 11;21(4):1207.PMID:32054089DOI:10.3390/ijms21041207.
Platycosides, the saponins abundant in Platycodi radix (the root of Platycodon grandiflorum), have diverse pharmacological activities and have been used as food supplements. Since deglycosylated saponins exhibit higher biological activity than glycosylated saponins, efforts are on to enzymatically convert glycosylated platycosides to deglycosylated platycosides; however, the lack of diversity and specificities of these enzymes has limited the kinds of platycosides that can be deglycosylated. In the present study, we examined the enzymatic conversion of platycosides and showed that Cytolase PCL5 completely converted platycoside E and polygalacin D3 into deapiose-xylosylated platycodin D and deapiose-xylosylated Polygalacin D, respectively, which were identified by LC-MS analysis. The platycoside substrates were hydrolyzed through the following novel hydrolytic pathways: platycoside E → platycodin D3 → platycodin D → deapiosylated platycodin D → deapiose-xylosylated platycodin D; and polygalacin D3 → Polygalacin D → deapiosylated Polygalacin D → deapiose-xylosylated Polygalacin D. Our results show that cytolast PCL5 may have a potential role in the development of biologically active platycosides that may be used for their diverse pharmacological activities.
Enzymatic Biotransformation of Balloon Flower Root Saponins into Bioactive Platycodin D by Deglucosylation with Caldicellulosiruptor bescii β-Glucosidase
Int J Mol Sci 2019 Aug 7;20(16):3854.PMID:31394870DOI:10.3390/ijms20163854.
Platycodin D (PD), a major saponin (platycoside) in Platycodi radix (balloon flower root), has higher pharmacological activity than the other major platycosides; however, its content in the plant root is only approximately 10% (w/w) and the productivities of PD by several enzymes are still too low for industrial applications. To rapidly increase the total PD content, the β-glucosidase from Caldicellulosiruptor bescii was used for the deglucosylation of the PD precursors platycoside E (PE) and platycodin D3 (PD3) in the root extract into PD. Under the optimized reaction conditions, the enzyme completely converted the PD precursors into PD with the highest productivity reported so far, increasing the total PD content to 48% (w/w). In the biotransformation process, the platycosides in Platycodi radix were hydrolyzed by four pathways: deapiosylated (deapi)-PE → deapi-PD3 → deapi-PD, PE → PD3 → PD, polygalacin D3 → Polygalacin D, and 3″-O-acetyl polygalacin D3 → 3″-O-acetyl Polygalacin D.
In addition to its endosomal escape effect, platycodin D also synergizes with ribosomal inactivation protein to induce apoptosis in hepatoma cells through AKT and MAPK signaling pathways
Chem Biol Interact 2022 Sep 1;364:110058.PMID:35872048DOI:10.1016/j.cbi.2022.110058.
Efficient endosomal escape after cellular uptake is a major challenge for the clinical application of therapeutic proteins. To overcome this obstacle, several strategies have been used to help protein drugs escape from endosomes without affecting the integrity of the cell membrane. Among them, some triterpenoid saponins with special structures were used to greatly enhance the anti-tumor therapeutic effect of protein toxins. Herein, we demonstrated that platycodin D (PD), Polygalacin D (PGD) and platycodin D2 (PD2) from Platycodonis Radix significantly enhanced the ability of MHBP (a type I ribosome-inactivating protein toxin MAP30 fused with a cell-penetrating peptide HBP) to induce apoptosis in hepatoma cells. Based on the results of co-localization of endocytosed EGFP-HBP with a lysosomal probe and Galectin-9 vesicle membrane damage sensor, we demonstrated that PD, PGD and PD2 have the ability to promote endosomal escape of endocytic proteins without affecting the integrity of the plasma membrane. Meanwhile, we observed that cholesterol metabolism plays an important role in the activity of PD by RNA-seq analysis and KEGG pathway enrichment analysis, and confirm that PD, PGD and PD2 enhance the anti-tumor activity of MHBP by inducing the redistribution of free cholesterol and inhibiting the activity of cathepsin B and cathepsin D. Finally, we found that PD synergized with MHBP to induce caspase-dependent apoptosis through inhibiting Akt and ERK1/2 signaling pathways and activating JNK and p38 MAPK signaling pathways. This study provides new insights into the application of PD in cancer therapy and provides efficient and promising strategies for the cytosolic delivery of therapeutic proteins.