Didymin
(Synonyms: 香风草甙) 目录号 : GC38179
A flavonoid with diverse biological activities
Cas No.:14259-47-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Didymin is a flavonoid that has been found in citrus fruits with diverse biological activities.1,2,3 It reduces hydrogen peroxide-induced production of reactive oxygen species (ROS) and cell death and increases superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity in SH-SY5Y cells differentiated into a neuronal phenotype.1 Didymin reduces survival of A549 and H460 lung cancer cells in a concentration-dependent manner via induction of cell cycle arrest at the G0/G1 phase and Fas-mediated apoptosis.2 In vivo, didymin (6 mg/kg) inhibits tumor growth in an A549 mouse xenograft model. It also reduces hepatic collagen deposition, the number of hepatic lesions, and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and TNF-α in a rat model of CCL4-induced hepatic fibrosis.3
1.Morelli, S., Piscioneri, A., Salerno, S., et al.Neuroprotective effect of didymin on hydrogen peroxide-induced injury in the neuronal membrane systemCells Tissues Organs199(2-3)184-200(2014) 2.Hung, J.-Y., Hsu, Y.-L., Ko, Y.-C., et al.Didymin, a dietary flavonoid glycoside from citrus fruits, induces Fas-mediated apoptotic pathway in human non-small-cell lung cancer cells in vitro and in vivoLung Cancer68(3)366-374(2010) 3.Lin, X., Bai, F., Nie, J., et al.Didymin alleviates hepatic fibrosis through inhibiting ERK and PI3K/Akt pathways via regulation of Raf kinase inhibitor proteinCell Physiol. Biochem.40(6)1422-1432(2016)
| Cas No. | 14259-47-3 | SDF | |
| 别名 | 香风草甙 | ||
| Canonical SMILES | O=C1C[C@@H](C2=CC=C(OC)C=C2)OC3=CC(O[C@H]4[C@@H]([C@H]([C@@H]([C@@H](CO[C@H]5[C@@H]([C@@H]([C@H]([C@H](C)O5)O)O)O)O4)O)O)O)=CC(O)=C13 | ||
| 分子式 | C28H34O14 | 分子量 | 594.56 |
| 溶解度 | DMSO: 250 mg/mL (420.48 mM) | 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 | 1.6819 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。
Didymin Suppresses Microglia Pyroptosis and Neuroinflammation Through the Asc/Caspase-1/GSDMD Pathway Following Experimental Intracerebral Hemorrhage
Front Immunol 2022 Jan 27;13:810582.PMID:35154128DOI:10.3389/fimmu.2022.810582.
Neuroinflammation has been proven to exert an important effect on brain injury after intracerebral hemorrhage (ICH). Previous studies reported that Didymin possessed anti-inflammatory properties after acute hepatic injury, hyperglycemia-induced endothelial dysfunction, and death. However, the role of Didymin in microglial pyroptosis and neuroinflammation after ICH is unclear. The current study aimed to investigate the effect of Didymin on neuroinflammation mediated by microglial pyroptosis in mouse models of ICH and shed some light on the underlying mechanisms. In this study, we observed that Didymin treatment remarkably improved neurobehavioral performance and decreased BBB disruption and brain water content. Microglial activation and neutrophil infiltration in the peri-hematoma tissue after ICH were strikingly mitigated by Didymin as well. At the molecular level, administration of Didymin significantly unregulated the expression of Rkip and downregulated the expression of pyroptotic molecules and inflammatory cytokines such as Nlrp3 inflammasome, GSDMD, caspase-1, and mature IL-1β, TNF-α, and MPO after ICH. Besides, Didymin treatment decreased the number of Caspase-1-positive microglia and GSDMD-positive microglia after ICH. Inversely, Locostatin, an Rkip-specific inhibitor, significantly abolished the anti-pyroptosis and anti-neuroinflammation effects of Didymin. Moreover, Rkip binding with Asc could interrupt the activation and assembly of the inflammasome. Mechanistically, inhibition of Caspase-1 by VX-765 attenuated brain injury and suppressed microglial pyroptosis and neuroinflammation by downregulation of GSDMD, mature IL-1β, TNF-α, and MPO based on Locostatin-treated ICH. Taken together, Didymin alleviated microglial pyroptosis and neuroinflammation, at least in part through the Asc/Caspase-1/GSDMD pathway via upregulating Rkip expression after ICH. Therefore, Didymin may be a potential agent to attenuate neuroinflammation via its anti-pyroptosis effect after ICH.
Didymin: an orally active citrus flavonoid for targeting neuroblastoma
Oncotarget 2017 Apr 25;8(17):29428-29441.PMID:28187004DOI:10.18632/oncotarget.15204.
Neuroblastoma, a rapidly growing yet treatment responsive cancer, is the third most common cancer of children and the most common solid tumor in infants. Unfortunately, neuroblastoma that has lost p53 function often has a highly treatment-resistant phenotype leading to tragic outcomes. In the context of neuroblastoma, the functions of p53 and MYCN (which is amplified in ~25% of neuroblastomas) are integrally linked because they are mutually transcriptionally regulated, and because they together regulate the catalytic activity of RNA polymerases. Didymin is a citrus-derived natural compound that kills p53 wild-type as well as drug-resistant p53-mutant neuroblastoma cells in culture. In addition, orally administered Didymin causes regression of neuroblastoma xenografts in mouse models, without toxicity to non-malignant cells, neural tissues, or neural stem cells. RKIP is a Raf-inhibitory protein that regulates MYCN activation, is transcriptionally upregulated by Didymin, and appears to play a key role in the anti-neuroblastoma actions of Didymin. In this review, we discuss how Didymin overcomes drug-resistance in p53-mutant neuroblastoma through RKIP-mediated inhibition of MYCN and its effects on GRK2, PKCs, Let-7 micro-RNA, and clathrin-dependent endocytosis by Raf-dependent and -independent mechanisms. In addition, we will discuss studies supporting potential clinical impact and translation of Didymin as a low cost, safe, and effective oral agent that could change the current treatment paradigm for refractory neuroblastoma.
Didymin Alleviates Cerebral Ischemia-Reperfusion Injury by Activating the PPAR Signaling Pathway
Yonsei Med J 2022 Oct;63(10):956-965.PMID:36168249DOI:10.3349/ymj.2022.0040.
Purpose: Cerebral ischemia-reperfusion (IR) injury is a severe secondary injury induced by reperfusion after stroke. Didymin has been reported to have a protective effect on intracerebral hemorrhage. However, the underlying mechanism of Didymin on regulating cerebral IR injury remains largely unknown. Materials and methods: A rat cerebral IR model and oxygen-glucose deprivation/reperfusion (OGD/R) model in PC12 cells were established. Hematoxylin and eosin (H&E) was used to detect the pathological changes in brain tissues, and TUNEL staining was performed to detect apoptosis of brain tissues. MTT and flow cytometry were used to measure the viability and apoptosis of PC12 cells. QRT-PCR and western blot were used to detect inflammation cytokines in PC12 cells. Western blot was used to measure the expression of PPAR-γ, RXRA, Bax, c-caspase-3, and Bcl-2. Results: Didymin pretreatment decreased apoptotic rates, reduced levels of Bax and c-caspase-3, and increased Bcl-2 level in vivo and in vitro. Additionally, Didymin pretreatment increased viability and decreased the inflammation levels [interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and monocyte chemotactic protein (MCP)-1] of OGD/R treated PC12 cells. Moreover, Didymin activated the peroxisome proliferator-activated receptors (PPAR) signaling pathway and increased the expression of PPAR-γ and RXRA in OGD/R treated PC12 cells. Inhibition of PPAR-γ eliminated the protective effect of Didymin on OGD/R treated cells. Conclusion: Didymin protected neuron cells against IR injury in vitro and in vivo by activation of the PPAR pathway. Didymin may be a candidate drug for IR treatment.
Didymin improves UV irradiation resistance in C. elegans
PeerJ 2019 Jan 9;6:e6218.PMID:30643686DOI:10.7717/peerj.6218.
Didymin, a type of flavono-o-glycoside compound naturally present in citrus fruits, has been reported to be an effective anticancer agent. However, its effects on stress resistance are unclear. In this study, we treated Caenorhabditis elegans with Didymin at several concentrations. We found that Didymin reduced the effects of UV stressor on nematodes by decreasing reactive oxygen species levels and increasing superoxide dismutase (SOD) activity. Furthermore, we found that specific didymin-treated mutant nematodes daf-16(mu86) & daf-2(e1370), daf-16(mu86), akt-1(ok525), akt-2(ok393), and age-1(hx546) were susceptible to UV irradiation, whereas daf-2(e1371) was resistant to UV irradiation. In addition, we found that Didymin not only promoted DAF-16 to transfer from cytoplasm to nucleus, but also increased both protein and mRNA expression levels of SOD-3 and HSP-16.2 after UV irradiation. Our results show that Didymin affects UV irradiation resistance and it may act on daf-2 to regulate downstream genes through the insulin/IGF-1-like signaling pathway.
Didymin attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress
Chin Herb Med 2021 Jul 15;14(1):70-78.PMID:36120130DOI:10.1016/j.chmed.2021.07.002.
Objective: This study was designed to investigate the protective effects of Didymin (Did) on doxorubicin (DOX)-induced cardiotoxicity. Methods: After pretreatment with Did (2, 4, 8 mg/kg intraperitoneal i.p.) for 7 d, the male C57 mice were injected with single dose of DOX (20 mg/kg i.p.). The cardioprotective effect of Did was observed on the 7th day after DOX treatment. Results: DOX delayed body growth and caused cardiac tissue injury, oxidative stress, and mitochondrial dysfunction. Similar experiments in H9C2 cardiomyocytes showed that DOX reduced cell viability, increased generation of reactive oxygen species (ROS) and fragmentation of DNA, decreased mitochondrial membrane potential, and induced cardiomyocyte apoptosis. However, all of these adverse effects were suppressed by Did pretreatment. Did increased protein expression of glutamate-L-cysteine ligase catalytic subunit (GCL), heme oxygenase 1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2). Besides, Did also induced activation of PI3K/AKT. Conclusion: These findings indicated Did prevented DOX-induced cardiac injury and apoptosis via activating PI3K/AKT/Nrf2 signaling pathway.