Paeoniflorigenone
(Synonyms: 芍药甙元酮) 目录号 : GC61799
Paeoniflorigenone是从牡丹皮中提取的一种有效成分，具有选择性诱导肿瘤细胞凋亡(apoptosis)和抗增殖作用。
Cas No.:80454-42-8
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Paeoniflorigenone, isolated as an active ingredient from the root of moutan cortex, induces apoptosis selectively in the cancer cell lines and exhibits antiproliferative effect[1].
Paeoniflorigenone (0-30 μM; 0-72 hours) significantly decreases the cell proliferation of tumor cell lines and inhibits the proliferation of normal cell lines[1].Paeoniflorigenone (0-30 μM; 24-72 hours) significantly induces apoptotic DNA fragmentation selectively in tumor cells[1]. Cell Proliferation Assay[1] Cell Line: TIG-1, 3T3-L1, HL60, Jurkat and HeLa cells
[1]. Huang Y, et al. Apoptosis-inducing activity and antiproliferative effect of Paeoniflorigenone from moutan cortex. Biosci Biotechnol Biochem. 2017;81(6):1106-1113.
| Cas No. | 80454-42-8 | SDF | |
| 别名 | 芍药甙元酮 | ||
| Canonical SMILES | O=C(C1=CC=CC=C1)OC[C@H]2[C@@H]3O[C@@]4(C[C@H]2C(C[C@@]4(O3)C)=O)O | ||
| 分子式 | C17H18O6 | 分子量 | 318.32 |
| 溶解度 | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 3.1415 mL | 15.7075 mL | 31.4149 mL |
| 5 mM | 0.6283 mL | 3.1415 mL | 6.283 mL |
| 10 mM | 0.3141 mL | 1.5707 mL | 3.1415 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。
Paeoniflorigenone regulates apoptosis, autophagy, and necroptosis to induce anti-cancer bioactivities in human head and neck squamous cell carcinomas
J Ethnopharmacol 2022 Apr 24;288:115000.PMID:35051602DOI:10.1016/j.jep.2022.115000.
Ethnopharmacological relevance: Paonia suffruticosa Andr. belonging to the family Paeoniaceae and has been used as a medicinal plant in Asian countries including China, Korea, and Japan. The roots of P. suffruticosa has been used in traditional medicine in various diseases including cancer and cardiovascular, female genital, and inflammatory diseases. Aim of the study: Head and neck squamous cell carcinomas (HNSCCs) pathologically account for 90% of all head and neck cancers. However, effective targeted therapies for HNSCCs are insufficient and the prognosis is very poor, especially in patients with metastatic HNSCCs. To overcome the current limitations of available therapies for HNSCCs, pathological approaches using natural compounds are attracting attention. Our study aimed to demonstrate the anti-cancer effects of Paeoniflorigenone (Paeo, 98.9% purity) isolated from the root bark of P. suffruticosa. Materials and methods: Our scientific methodology was performed as follows: cytotoxicity, morphological changes, and apototic DNA fragmentation were analyzed using MTT, light microscopy, and TUNEL assays. Protein expression, apoptosis, necroptosis, and autophagy were analyzed using Western blot and immunofluorescence assays. Cell migration and invasion were analyzed using wound healing and Boyden chamber assays. Results: We demonstrated that Paeo significantly reduced cell proliferation and cell division, leading to caspase-dependent apoptotic cell death in human YD-10B HNSCC cells. This result was associated with PI3K/AKT/mTOR/p70S6K signaling in these cells. In addition, we investigated other programmed cell death mechanisms associated with apoptosis and found that Paeo inhibited necroptosis via dephosphorylation of key necroptotic proteins (RIP and MLKL), whereas Paeo induced autophagy via increased LC3I/II expression and autophagosome formation in human YD-10B HNSCC cells. The anti-metastatic effects of Paeo significantly suppressed cell migration and invasion in human YD-10B HNSCC cells. Conclusion: Overall, our results demonstrated that the bioactive compound, Paeo, exhibited anti-cancer bioactivities in human YD-10B HNSCC cells, suggesting that Paeo may be an attractive pathological approach for patients with human HNSCCs.
Apoptosis-inducing activity and antiproliferative effect of Paeoniflorigenone from moutan cortex
Biosci Biotechnol Biochem 2017 Jun;81(6):1106-1113.PMID:28317437DOI:10.1080/09168451.2017.1300517.
Ninety samples from the extracts of plants from traditional Chinese medicines were screened for antitumor activity. Paeoniflorigenone (PFG) was isolated as an active ingredient from the root of moutan cortex, which showed the strongest activity. In addition, our data indicated that PFG was cytotoxic and induced apoptosis selectively in the cancer cell lines. These effects were cancelled by the addition of caspase inhibitor Z-VAD-FMK, suggesting that it was mediated by caspase-3 activation.
Blocking effects of a new component, Paeoniflorigenone, in paeony root on neuromuscular junctions of frogs and mice
Jpn J Pharmacol 1984 May;35(1):61-6.PMID:6471620DOI:10.1254/jjp.35.61.
A new monoterpene, Paeoniflorigenone (PFG) (100-900 micrograms/ml), which was isolated from paeony roots and identified chemically, suppressed both indirectly and directly stimulated muscle twitchings of frog sciatic nerve-sartorius muscle preparation, and it indirectly stimulated muscle twitchings of phrenic nerve-diaphragm muscle preparations. The suppression effect by PFG (300 micrograms/ml) on twitching was not reversed by neostigmine (60 micrograms/ml) and was restored by washing out of PFG. PFG (150 micrograms/ml) depolarized the diaphragm muscle membranes by 10 mV and did not change the electrotonic potentials. PFG (100 micrograms/ml) inhibited weakly acetylcholine (5 micrograms/ml)-induced slow contractions. These results demonstrated that PFG is a depolarizing neuromuscular blocking agent, being similar to succinylcholine, except that PFG did not produce any contraction, but succinylcholine did.
Protective Roles of Xijiao Dihuang Tang on Coronary Artery Injury in Kawasaki Disease
Cardiovasc Drugs Ther 2023 Apr;37(2):257-270.PMID:34665368DOI:10.1007/s10557-021-07277-w.
Purpose: Xijiao Dihuang Tang (XJDHT) is a classical formula of traditional Chinese medicine constituted of Cornu Bubali, Rehmannia glutinosa (Gaertn.) DC., Paeonia lactiflora Pall., and Paeonia suffruticosa Andrews. It was first mentioned in the medical classic "Beiji Qianjin Yaofang" written by Simiao Sun in Tang Dynasty. It shows very strong antipyretic and anticoagulant effects and has been clinically applied to treat various type of blood loss, purple and black spots, heat stroke, and glossitis. Kawasaki disease (KD) is considered as a kind of acute febrile illness in children with systemic vasculitis as the main lesions. The aim of this research is to clarify whether XJDHT can play a protective role in KD. Methods: A mouse model of Candida albicans water-soluble fraction (CAWS)-induced coronary arteritis and a KD cell model with tumor necrosis factor (TNF)-α induction were employed to investigate the potential effect and mechanism of XJDHT on coronary artery injury in KD. Results: Data showed that XJDHT remarkably alleviated the coronary artery injury of KD mice, as evidenced by reduced inflammation and downregulated expression of pro-inflammatory cytokines interleukin (IL)-1β and TNF-α. In vitro investigation showed that XJDHT could promote cell proliferation, inhibit cell apoptosis, and improve mitochondrial functions. Subsequent studies demonstrated that XJDHT rescued endothelial cell injury by PI3K/Akt-NFκB signaling pathway. Component analysis of XJDHT detected thirty-eight chemically active ingredients, including paeoniflorin, albiflorin, and Paeoniflorigenone, which in in vitro experiments exhibited significant rescue effects on TNF-α-mediated endothelial cell injury. Conclusion: Our findings demonstrated that XJDHT mitigated coronary artery injury of KD through suppressing endothelial cell damage via PI3K/Akt-NFκB signaling.
High-Throughput Chinmedomics Strategy Discovers the Quality Markers and Mechanisms of Wutou Decoction Therapeutic for Rheumatoid Arthritis
Front Pharmacol 2022 Apr 12;13:854087.PMID:35496313DOI:10.3389/fphar.2022.854087.
Wutou decoction (WTD) is a traditional Chinese medicine prescription for the treatment of rheumatoid arthritis (RA), and this study systematically analyzed the metabolic mechanism and key pharmacodynamic components of WTD in RA rats by combining untargeted metabolomics and serum pharmacochemistry of traditional Chinese medicine to enrich the evidence of WTD quality markers (Q-markers) studies. WTD prevented synovial edema in RA rats and reduced tumor necrosis factor-alpha and interleukin 6 levels in rat serum, according to the results of an enzyme-linked immunosorbent examination and histopathological inspection. In model rats, pattern recognition and multivariate statistical analysis revealed 24 aberrant metabolites that disrupted linoleic acid metabolism, arachidonic acid metabolism, arginine and proline metabolism, etc. However, continued dosing of WTD for 28 days reversed 13 abnormal metabolites, which may be an important therapeutic mechanism from a metabolomic perspective. Importantly, 12 prototypical components and 16 metabolites from WTD were characterized in RA rat serum. The results of Pearson correlation analysis showed that aconitine, L-ephedrine, L-methylephedrine, quercetin, albiflorin, Paeoniflorigenone, astragaline A, astragaloside II, glycyrrhetic acid, glycyrrhizic acid, licurazide, and isoliquiritigenin are the key pharmacological components that regulate the metabolism of RA rats, and they are identified as Q-markers. In sum, utilizing metabolomics and serum pharmacochemistry of traditional Chinese medicine, the metabolic mechanisms and Q-markers of WTD therapy in RA rats were revealed, providing a theoretical basis for the quality control investigation of WTD.