Poncirin
(Synonyms: 枸橘甙) 目录号 : GC39069
A flavonoid glycoside with diverse biological activities
Cas No.:14941-08-3
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
Poncirin is a flavonoid glycoside that has been found in P. trifoliata and has diverse biological activities.1,2,3,4 It inhibits the growth of SGC-7901 gastric cancer cells when used at concentrations ranging from 5 to 25 ?g/ml.2 Poncirin (25-100 ?M) inhibits LPS-induced NF-κB DNA-binding activity, as well as production of nitric oxide (NO) and prostaglandin E2 in RAW 264.7 cells.3 It reduces the gastric ulcer lesion index in a rat model of HCl/ethanol-induced gastritis when administered at doses of 50 and 100 mg/kg.4
1.Mouly, P., Gaydou, E.M., and Auffray, A.Simultaneous separation of flavanone glycosides and polymethoxylated flavones in citrus juices using liquid chromatographyJ. Chromatogr. A800(2)171-179(1998) 2.Zhu, X., Luo, F., Zheng, Y., et al.Characterization, purification of Poncirin from edible Citrus Ougan (Citrus reticulate cv. Suavissima) and its growth inhibitory effect on human gastric cancer cells SGC-7901Int. J. Mol. Sci.14(5)8684-8697(2013) 3.Kim, J.-B., Han, A.-R., Park, E.-Y., et al.Inhibition of LPS-induced iNOS, COX-2 and cytokines expression by poncirin through the NF-κB inactivation in RAW 264.7 macrophage cellsBiol. Pharm. Bull.30(12)2345-2351(2007) 4.Lee, J.-H., Lee, S.-H., Kim, Y.S., et al.Protective effects of neohesperidin and poncirin isolated from the fruits of Poncirus trifoliata on potential gastric diseasePhytother. Res.23(12)1748-1753(2009)
| Cas No. | 14941-08-3 | SDF | |
| 别名 | 枸橘甙 | ||
| Canonical SMILES | O=C(C[C@@H](C1=CC=C(OC)C=C1)OC2=CC(O[C@H](O[C@H](CO)[C@@H](O)[C@@H]3O)[C@@H]3O[C@@](O[C@@H](C)[C@H](O)[C@H]4O)([H])[C@@H]4O)=C5)C2=C5O | ||
| 分子式 | C28H34O14 | 分子量 | 594.56 |
| 溶解度 | Water: >10 mg/mL | 储存条件 | Store at -20°C |
| 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 | 1.6819 mL | 8.4096 mL | 16.8192 mL |
| 5 mM | 0.3364 mL | 1.6819 mL | 3.3638 mL |
| 10 mM | 0.1682 mL | 0.841 mL | 1.6819 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。
Poncirin ameliorates cardiac ischemia-reperfusion injury by activating PI3K/AKT/PGC-1α signaling
Eur J Pharmacol 2022 Feb 15;917:174759.PMID:35032487DOI:10.1016/j.ejphar.2022.174759.
Poncirin, a flavonoid glycoside derivative extracted from the fruits of Poncirus trifoliata (trifoliate orange or Chinese bitter orange), has a variety of documented bioactivities, including anti-tumor, anti-inflammatory, and antioxidant effects. Oxidative stress is a major underlying factor in the pathogenesis of cardiac ischemia-reperfusion (I/R) injury. Therefore, we investigated the protective efficacy of Poncirin on primary cardiomyocytes subjected to anoxia-reoxygenation (A/R) injury in vitro, and on rat hearts subjected to ischemia-reperfusion (I/R) injury in vivo. Poncirin pretreatment enhanced cardiomyocyte survival, inhibited A/R-induced oxidative stress by upregulating cellular antioxidant capacity, suppressed mitochondrial depolarization, and ultimately inhibited apoptosis. Similarly, systemic Poncirin treatment significantly reduced cardiomyocyte apoptosis and infarct size in rat hearts. In addition, activity of the PI3K/AKT/PGC-1α pathway was significantly increased by Poncirin pretreatment in both A/R and I/R injury models, while PI3K and PGC-1α inhibitors abolished all Poncirin related effects, suggesting that this pathway is essential for the cardioprotective effects of Poncirin. Pretreatment with the PGC-1α inhibitor reversed effects of Poncirin without affecting p-AKT expression, indicating that PGC-1α is downstream of AKT. In conclusion, both in vitro and in vivo studies suggested that Poncirin alleviates cardiac ischemia-reperfusion injury by mitigating oxidative stress, which is dependent on activation of the PI3K/AKT/PGC-1α signaling pathway.
Poncirin ameliorates oxygen glucose deprivation/reperfusion injury in cortical neurons via inhibiting NOX4-mediated NLRP3 inflammasome activation
Int Immunopharmacol 2022 Jan;102:107210.PMID:34266770DOI:10.1016/j.intimp.2020.107210.
Poncirin, a natural flavonoid present abundantly in citrus fruits, possesses anti-oxidant and anti-inflammatory activities that contribute to neuroprotection, but its roles and mechanisms in neuronal injury is still poorly understood. In this study, an oxygen-glucose deprivation/reoxygenation (OGD/R) model was established in primary cortical neurons to induce neuronal injury in vitro. Poncirin effectively attenuated OGD/R-induced neuronal damage by enhancing cell viability, restraining lactate dehydrogenase release, and reducing apoptosis of neurons. Poncirin restrained mitochondrial dysfunction and oxidative stress by increasing mitochondrial membrane potential, declining reactive oxygen species production, lessening malondialdehyde generation, and increasing the activities of antioxidant enzymes in OGD/R-treated neurons. Poncirin also repressed inflammatory responses by reducing the secretion of pro-inflammatory factors, and inhibiting NLRP3 inflammasome activation. Importantly, Poncirin administration notably abolished OGD/R-induced upregulation of NADPH oxidase 4 (NOX4), and overexpression of NOX4 neutralized poncirin-mediated neuroprotection. In conclusion, Poncirin protects cortical neurons from OGD/R injury via inhibiting NOX4/ROS/NLRP3 axis.
Poncirin downregulates ATP-binding cassette transporters to enhance cisplatin sensitivity in cisplatin-resistant osteosarcoma cells
Phytother Res 2021 Jan;35(1):278-288.PMID:32779800DOI:10.1002/ptr.6798.
Poncirin, a flavanone glycoside with bitter taste extracted from dried immature fruit of Poncirus trifoliate, exhibits multiple biological activities including anti-tumor activity. Our study aimed to determine the effect and potential mechanism of Poncirin on cisplatin resistance in osteosarcoma (OS) cells. CCK-8, flow cytometry analysis, and caspase-3/7 activity assays were used to evaluate cisplatin sensitivity. The expression changes of multidrug resistance 1 (MDR1), multidrug resistance-associated protein (MRP1), breast cancer resistance protein (BCRP), and phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) pathway-related proteins were detected by RT-qPCR or western blot analyses. Results showed that Poncirin exposure enhanced cisplatin sensitivity, promoted apoptosis, and increased caspase-3/7 activity in cisplatin-resistant OS cells. Poncirin decreased the expression levels of MDR1, MRP1, and BCRP, and inhibited the PI3K/Akt signaling in OS cells. Rescue experiments suggested that activation of the PI3K/Akt signaling by 740Y-P abolished poncirin-induced expression reduction of MDR1, MRP1, and BCRP, and attenuated the facilitative effects of Poncirin on cisplatin sensitivity and apoptosis in cisplatin-resistant OS cells. In summary, Poncirin suppressed cisplatin resistance in cisplatin-resistant OS cells by downregulating the expression of MDR1, MRP1, and BCRP through inhibiting the PI3K/Akt pathway.
Poncirin attenuates CCL4-induced liver injury through inhibition of oxidative stress and inflammatory cytokines in mice
BMC Complement Med Ther 2020 Apr 19;20(1):115.PMID:32307011DOI:10.1186/s12906-020-02906-7.
Background: In the present study, the Poncirin which is flavonoid-7-o-glycosides (isolated from the Poncirus trifoliata) in nature was evaluated against the Carbon tetra chloride (CCL4)-induced liver injury. The Poncirin have been reported for various anti-inflammatory, analgesic activity etc. Based on the previous studies it was anticipated that the Poncirin will ameliorate CCL4-induced liver injury. Methods: The CCL4-induced acute and chronic liver injury model (albino BALB/c mice) was used. Following the induction of the liver injury various parameters such as food and water intake, body weight and weight to dry ratio changes were assessed. Furthermore, various hematological, biochemical parameters and histological studies such as hemotoxylin and eosin (H and E) staining were performed. The Poncirin treatment was also evaluated against the pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) using enzyme link immunosorbant assay (ELISA). The Swiss Target prediction software was used to investigate interaction of the Poncirin on the various hepatic enzymes. Results: The Poncirin treatment markedly improved the behavioral parameters such as food and water intake. The liver weight variation was attenuated and total body was improved markedly. The hematological and biochemical parameters were significantly improved compared to the CCL4 treated groups. The anti-oxidants were induced, while oxidative stress markers were reduced promisingly. The H and E staining showed that Poncirin treatment significantly improved the histology of liver compared to the CCL4 treated group. Furthermore, the Poncirin treatment also evidently decreased the inflammatory mediators. Conclusions: The Poncirin treatment showed marked improvement in behavioral, biochemical and histological parameters following CCL4-induced liver injury. Additionally, the Poncirin treatment also markedly improved the antioxidant enzymes, attenuated the oxidative stress markers and inflammatory cytokines.
Poncirin Inhibits Osteoclast Differentiation and Bone Loss through Down-Regulation of NFATc1 In Vitro and In Vivo
Biomol Ther (Seoul) 2020 Jul 1;28(4):337-343.PMID:31500404DOI:10.4062/biomolther.2018.216.
Activation of osteoclast and inactivation of osteoblast result in loss of bone mass with bone resorption, leading to the pathological progression of osteoporosis. The receptor activator of NF-κB ligand (RANKL) is a member of the TNF superfamily, and is a key mediator of osteoclast differentiation. A flavanone glycoside isolated from the fruit of Poncirus trifoliata, Poncirin has anti-allergic, hypocholesterolemic, anti-inflammatory and anti-platelet activities. The present study investigates the effect of Poncirin on osteoclast differentiation of RANKL-stimulated RAW264.7 cells. We observed reduced formation of RANKL-stimulated TRAP-positive multinucleated cells (a morphological feature of osteoclasts) after Poncirin exposure. Real-time qPCR analysis showed suppression of the RANKL-mediated induction of key osteoclastogenic molecules such as NFATc1, TRAP, c-Fos, MMP9 and cathepsin K after Poncirin treatment. Poncirin also inhibited the RANKL-mediated activation of NF-κB and, notably, JNK, without changes in ERK and p38 expression in RAW264.7 cells. Furthermore, we assessed the in vivo efficacy of Poncirin in the lipopolysaccharide (LPS)-induced bone erosion model. Evaluating the micro-CT of femurs revealed that bone erosion in Poncirin treated mice was markedly attenuated. Our results indicate that Poncirin exerts anti-osteoclastic effects in vitro and in vivo by suppressing osteoclast differentiation. We believe that Poncirin is a promising candidate for inflammatory bone loss therapeutics.