Deltonin
(Synonyms: 三角叶薯蓣皂苷) 目录号 : GC32254
Deltonin是从盾叶薯蓣中得到的甾体皂苷，能够抑制ERK1/2和AKT的活化，具有抗肿瘤的活性。
Cas No.:55659-75-1
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
Cell experiment: | The cytotoxicity of Deltonin on colon cancer cells is determined by the MTT assay. Cells are seeded at a density of 3 × 103 per well in 96-well plates. After incubation overnight, cells are treated with Deltonin in various concentrations (0.5, 1, 2, 4, 8 μM), and carrier DMSO (< 0.05%) is used as a control, 5 wells are included in each concentration. Every 24 h the absorbance at 570 nm is measured with SpectraMax M5, using wells without cells as blanks. All experiments are performed in triplicate. The concentration-and time-dependent curves of the Deltonin-treated colon cancer cell lines is generated as the % cell growth inhibition, using the following formula: % inhibition = (A570 of control - A570 of treated cells)/A570 of control cells × 100%. The 50% inhibiting concentration (IC50) is calculated[1]. |
Animal experiment: | Mice[1]Briefly, 5 × 105 C26 cells are s.c. injected into 4- to 6-wk-old male BALB/c mice. The mice are randomly divided into four groups of 10 mice. One week after C26 implantation, the treatment groups receive their first doses of Deltonin dissolved in a vehicle solution of DMSO (< 0.1%) and diluted in saline solution. Briefly, Deltonin is given via oral administration to tumor-bearing mice at 10, 20 and 40 mg/kg every day for 3 weeks (between day 8 and 28). In parallel, the control group receives the vehicle (DMSO, < 0.1%) in saline solution. The same quantity of saline solution containing DMSO is used in these groups. General clinical observations of the mice, including determination of body weight and tumor growth, are made twice weekly. To determine tumor size, two perpendicular diameters of the tumor in centimeters is measured by calipers. Tumor volume is estimated using the formula 0.52 × a × b2, where “a” is the long diameter and “b” is the short diameter. The mice are sacrificed when they become moribund, and the sacrifice date is recorded to calculate the survival time. To detect the apoptosis protein expression and microvessel density, tumor tissues are removed, fixed in 10% formalin or not and snap-frozen in liquid nitrogen immediately[1]. |
References: [1]. Tong QY, et al. Deltonin, a steroidal saponin, inhibits colon cancer cell growth in vitro and tumor growth in vivo via induction of apoptosis and antiangiogenesis. Cell Physiol Biochem. 2011;27(3-4):233-42. | |
Deltonin, a steroidal saponin, isolated from Dioscorea zingiberensis Wright, with antitumor activity; Deltonin inhibits ERK1/2 and AKT activation.
Deltonin inhibits ERK1/2 and AKT activation. Deltonin (0.5-8 μM) significantly inhibits the proliferation of several colon cancer cell lines including SW480, SW620, LOVO and C26, with IC50s of 1.3, 1.29, 2.11 and 1.22 μM. Deltonin also causes G2-M phase arrest and induces apoptosis in C26 cells[1]. Deltonin (0-5 μM) decreases the phosphorylation of AKT and ERK1/2 levels in MDA?MB?231 cells. Deltonin (0.5-8 μM) also dose-dependently inhibits the proliferation, and causes apoptosis with ROS production in MDA?MB?231 cells[2].
Deltonin (20 and 40 mg/kg, p.o.) reduces the tumor growth of 37.7% and 56.7%, and causes a 50-day survival rate of 60% and 50%, respectively, in mice. Deltonin also inhibits tumor angiogenesis in mice[1].
[1]. Tong QY, et al. Deltonin, a steroidal saponin, inhibits colon cancer cell growth in vitro and tumor growth in vivo via induction of apoptosis and antiangiogenesis. Cell Physiol Biochem. 2011;27(3-4):233-42. [2]. Zhang S, et al. Deltonin induces apoptosis in MDA?MB?231 human breast cancer cells via reactive oxygen species?mediated mitochondrial dysfunction and ERK/AKT signaling pathways. Mol Med Rep. 2013 Mar;7(3):1038-44.
| Cas No. | 55659-75-1 | SDF | |
| 别名 | 三角叶薯蓣皂苷 | ||
| 分子式 | 分子量 | ||
| 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。 |
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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。 | ||
| 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。
Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation
Neuropsychiatr Dis Treat 2020 Mar 31;16:871-879.PMID:32280228DOI:10.2147/NDT.S227988.
Introduction: Deltonin, an active component extracted from Dioscorea zingiberensis C.H. WRIGHT, was widely utilized in traditional Chinese medicines. It has been shown to have anti-cancer functions such as colon cancer, breast cancer, and head and neck squamous carcinoma. Herein, we will investigate the role of Deltonin in cerebral ischemia/reperfusion injuries. Methods: Ly294002 and anisomycin were used as inhibitors to monitor the effects of Deltonin. Middle cerebral artery occlusion I/R model was constructed. Infarct volumes, neurological deficits and brain water contents were evaluated under different conditions. Rotarod test, ELISA, and Western blotting were carried to investigate the effects in vitro. Results: We found that Deltonin in ischemia/reperfusion (I/R) rats greatly enhanced brain damages as well as neurological functions through up-regulating p-Akt and p-mTOR as well as inhibiting the expressions of LC3-II/LC3-I, Beclin-1, IL-1, TLR4, and p-p38. Deltonin exerted neuroprotection effect through relieving autophagy activity by regulating PI3K/Akt/mTOR signaling. Deltonin suppressed inflammation reactions through modulation TLR4/p38/MAPK signaling as well. Conclusion: Overall, our data suggested that Deltonin could suppress ischemic brain injury by regulating autophagy and inflammation during I/R. Deltonin can be a potential therapeutic method for patient with I/R.
Deltonin induced both apoptosis and autophagy in head and neck squamous carcinoma FaDu cell
Neoplasma 2015;62(3):419-31.PMID:25866222DOI:10.4149/neo_2015_050.
For decades, despite the advancement of medical science, the prognosis of head and neck squamous cell carcinoma (HNSCC), has not improved. Deltonin is one of the major active components of Dioscorea Zingiberensis Wright that has been used for anthrax, rheumatic heart disease, rheumatoid arthritis etc. By employing HNSCC FaDu cell and normal human epidermal keratinocyte, we investigate Deltonin efficacy and associated mechanism in both cell culture and nude mice xenografts. Deltonin treatment selectively prevents proliferation of FaDu cells by cell-cycle arrest and induction of apoptosis, via activating checkpoint kinase Chk1and Chk2 as well as caspases 8, 9 and 3. Meanwhile, we found that treatment with Deltonin induced autophagy, which played a protective role against deltonin-induced apoptosis. Further studies revealed that Deltonin activated autophagy by Akt-mTOR signaling. Additionally, xenograft model showed that administration of Deltonin significantly inhibited tumor growth and prolonged survival of tumor bearing mice. Our studies suggested that Deltonin might be a potential chemotherapeutic agent against HNSCC, which might contribute to clinical application and pharmacological study of Deltonin in future anti-cancer research.
Determination of Deltonin in rat plasma by using HPLC-MS/MS and the application of this method in pharmacokinetic studies
J Chromatogr B Analyt Technol Biomed Life Sci 2013 Jul 15;931:1-5.PMID:23747424DOI:10.1016/j.jchromb.2013.05.005.
Deltonin is a naturally occurring spirostanol glycoside from Dioscorea zingiberensis C.H. Wright, which is used in traditional Chinese medicine. It exerts strong cytotoxic effect on C26 cells, inhibits C26 derived-tumor growth, and prolongs the survival of tumor-bearing mice after its oral administration, indicating its potential for use as an anti-tumor drug. To investigate the pharmacokinetic profiles of Deltonin, a rapid, sensitive, and simplified high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) assay was developed and validated for the determination of Deltonin in rat plasma. After acetonitrile-mediated plasma protein precipitation, chromatographic separation of Deltonin was achieved using a reversed phase Hypersil Gold column (150mm脳2.1mm, 5渭m), with gradient elution using 0.1% formic acid and acetonitrile. Thereafter, Deltonin was quantified using MS/MS with electrospray ionization (ESI) in positive multiple reaction monitoring (MRM) mode. The flow rate of the mobile phase was 200渭L/min, and the retention time was 9.03min for Deltonin and 6.31min for the internal standard (IS: 20(S)-ginsenoside Rb1). The linear range of the calibration curve was 2-5000ng/mL (r(2)>0.99), and the limit of detection (LOD) was 0.46ng/mL. The intra- and inter-day accuracies ranged from -2.8% to 11.1% and precisions (RSD) were within 13.1%. Deltonin was found to be stable under short-term temperature conditions, post-preparative temperature conditions, and after 3 freeze-thaw cycles conditions. The validated method was successfully applied to a pharmacokinetic study in rats after oral administration of Deltonin (50 and 100mg/kg). The pharmacokinetics is characterized by high apparent clearance (CL/F) and apparent volume of distribution (Vd/F).
Deltonin, a steroidal saponin, inhibits colon cancer cell growth in vitro and tumor growth in vivo via induction of apoptosis and antiangiogenesis
Cell Physiol Biochem 2011;27(3-4):233-42.PMID:21471712DOI:10.1159/000327949.
Deltonin, a steroidal saponin, isolated from Dioscorea zingiberensis Wright (DZW), has shown high-cytotoxic activity in cancer cells. However, its mechanisms and in vivo anti-cancer effects remain unknown. In the present study, we evaluated the effects and explored the anti-tumor mechanisms of Deltonin on a panel of colon cancer cell lines and in a mouse model of murine colon cancer C26. Deltonin had more cytotoxic effect on C26 cells than 5-fluorouracil had, promoting dramatic G2-M phase arrest and apoptosis in C26 cells in a concentration-dependent manner; oral administration of Deltonin significantly inhibited the tumor growth and prolonged survival of the tumor bearing mice. The Deltonin treatment caused a noticeable apoptosis in tumor tissue, which associated with increased levels of Bax, activated caspase-3, caspase-9, and cleaved poly (ADPribose) polymerase, decreased pro-caspase-8, pro-caspase-9, Bcl-2 expression levels and extracellular signal-regulated kinase-1/2 activity; and dose-dependently inhibit angiogenesis. In conclusion, the findings in this study demonstrated that Deltonin is an effective natural agent for cancer therapy, which may be mediated, in part, by induction of apoptosis, as well as involve mitogen-activated protein kinase pathways, and inhibition of angiogenesis.
Deltonin induces apoptosis in MDA鈥慚B鈥?31 human breast cancer cells via reactive oxygen species鈥憁ediated mitochondrial dysfunction and ERK/AKT signaling pathways
Mol Med Rep 2013 Mar;7(3):1038-44.PMID:23314115DOI:10.3892/mmr.2013.1273.
Deltonin, a steroidal saponin isolated from Dioscorea zingiberensis Wright, exhibits high cytotoxic activity in cancer cells. In the present study, the effects of Deltonin on cell proliferation and apoptosis were evaluated in the MDA鈥慚B鈥?31 human breast carcinoma cell line. Following treatment with Deltonin, the viability of MDA鈥慚B鈥?31 cells was analyzed using MTT assay and apoptosis, mitochondrial membrane potential (鈭單╩) alternation and intracellular reactive oxygen species (ROS) generation was determined by flow cytometry. In addition, western blot analysis was performed to examine the expression of apoptosis鈥慳ssociated proteins. The results demonstrated that Deltonin induced apoptosis in MDA鈥慚B鈥?31 cells in a time鈥?and concentration鈥慸ependent manner. Apoptosis was associated with depolarization of 鈭單╩ and time鈥慸ependent ROS generation. Deltonin treatment also resulted in Bax upregulation, Bcl-2 downregulation, activation of caspase鈥? and 鈥? and poly (ADP ribose) polymerase cleavage. Decreased levels of phosphorylated extracellular signal鈥憆egulated kinase (ERK) and phosphorylated AKT were also observed. Results indicate that the proliferation inhibitory effect of Deltonin is associated with its apoptosis鈥慽nducing effect, which may correlate with ROS鈥憁ediated mitochondrial dysfunction as well as activation of the ERK/AKT signaling pathways. Therefore, Deltonin may be a potential chemotherapeutic agent for the treatment of breast cancer.