Strophanthidin
(Synonyms: 葡萄球菌素) 目录号 : GC63832
Strophanthidin 是一种天然的心脏糖苷。Strophanthidin 0.1 和 1 nmol/L 增加 Na+/K+-ATPase 活性，1~100 μ mol/L 抑制 Na+/K+-ATPase 活性，而 Strophanthidin 10 和 100 nmol/L 对 Na+/K+-ATPase活性无影响。Strophanthidin 增加舒张期和收缩期胞内 Ca2+ 浓度。
Cas No.:66-28-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >92.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Strophanthidin is a naturally available cardiac glycoside[1]. Strophanthidin 0.1 and 1 nmol/L increases and 1~100 µmol/L inhibits the Na+/K+-ATPase activities, but Strophanthidin 10 and 100 nmol/L does not affect Na+/K+-ATPase activities in cardiac sarcolemmal[2]. Strophanthidin increases both diastolic and systolic intracellular Ca2+ concentration[3].
Strophanthidin (0~10 μM; 24 hours; MCF-7, A549, and HepG2 cells) is effective at suppressing the growth of cancer cells and has no toxicity in normal cells[1].Strophanthidin (0.5 to 500 µM; PBMCs) does not show significant cytotoxicity in PBMCs. Strophanthidin (2 µM; MCF-7 cells) can arrest cell cycle at the G2/M phase[1].Strophanthidin (MCF-7, A549, and HepG2 cells) is effective at suppressing the growth of cancer cells and has no toxicity in normal cells. Strophanthidin (MCF-7, A549, and HepG2 cells) inhibits the expression of checkpoint and cyclin-dependent kinases in three cancer cells compared to untreated controls. Strophanthidin can modulate the protein localization from the nucleus to the membrane as well as to the cytoplasm. Strophanthidin is a monosaccharide cardiac glycoside with one aglycone portion and without any sugar unit. Strophanthidin induces apoptosis by the attenuation of multiple biochemical signaling pathways and by arresting cell cycle at the G2/M phase through p53-dependent and p53-independent mechanisms[1].
[1]. Reddy D, et al. Strophanthidin Attenuates MAPK, PI3K/AKT/mTOR, and Wnt/β-Catenin Signaling Pathways in Human Cancers. Front Oncol. 2020;9:1469. Published 2020 Jan 17.
[2]. Su SW, et al. Relationship between cardiotonic effects and inhibition on cardiac sarcolemmal Na+,K+-ATPase of strophan-thidin at low concentrations. Acta Pharmacol Sin. 2003;24(11):1103-1107.
[3]. Bennett DL, et al. Strophanthidin-induced gain of Ca2+ occurs during diastole and not systole in guinea-pig ventricular myocytes. Pflugers Arch. 1999;437(5):731-736.
| Cas No. | 66-28-4 | SDF | Download SDF |
| 别名 | 葡萄球菌素 | ||
| 分子式 | C23H32O6 | 分子量 | 404.5 |
| 溶解度 | Ethanol : 25 mg/mL (61.80 mM; Need ultrasonic) | 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 | 2.4722 mL | 12.3609 mL | 24.7219 mL |
| 5 mM | 0.4944 mL | 2.4722 mL | 4.9444 mL |
| 10 mM | 0.2472 mL | 1.2361 mL | 2.4722 mL |
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2.
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Acaricidal activity of Strophanthidin derivatives against Psoroptes cuniculi and their inhibitory effect on Na+-K+-ATPase
Vet Parasitol 2021 Aug;296:109498.PMID:34139615DOI:10.1016/j.vetpar.2021.109498.
In our previous studies, we found that as the active gradients of Adonis coerulea, cardenolides and cardiac glycosides presented toxicity against mites by inhibiting Na+-K+-ATPase. In this paper, after evaluating the acaricidal activity of the commercial cardiac aglycones/glycosides, serials of novel Strophanthidin derivatives were designed and synthesized with an efficient and simple route under mild conditions, and their toxicity against mites, the cytotoxicity and inhibitory effect on Na+-K+-ATP enzyme in PC12 cells were investigated. Results showed among of all compounds, including 9 commercial agent and 32 synthesized Strophanthidin derivatives, QXG-1 presented the strongest toxicity against mites with the LC50 value of 320.0 μg/mL. C-19 group of Strophanthidin substituted with glycinemethylester would increase the toxicity against mites, and the hydroxyl group at C-5 play the vital role in terms of the toxicity. At the given concentration, QXG-1 displayed the safety against PC12 (10.0 μg/mL) in vitro and mice (3.2 mg/kg) in acute toxicity test, and strong inhibitory effect on Na+-K+-ATPase. It could be used as a promising acaricidal agent. This study lays the foundation to develop of QXG-1 as a relatively safe and alternative acaricidal agent.
The effect of Strophanthidin on action potential, calcium current and contraction in isolated guinea-pig ventricular myocytes
J Physiol 1991 Nov;443:1-23.PMID:1822522DOI:10.1113/jphysiol.1991.sp018819.
1. A method is described for producing high yields of calcium-tolerant ventricular myocytes from guinea-pig hearts (73.4% rod-shaped cells, n = 19). Their action potential (AP) and membrane currents were recorded using conventional microelectrodes and cell shortening was measured optically using a linear photodiode array. 2. The sensitivity of the guinea-pig Na(+)-K+ pump to Strophanthidin (a rapidly acting digitalis analogue) was determined by measuring the inhibition of outward pump current by different doses. The pump was found to have a dissociation constant (KD) for Strophanthidin of 1.11 x 10(-5) M, and 5 x 10(-4) M-strophanthidin inhibited the pump maximally. 3. Exposure to Strophanthidin resulted in an initial lengthening followed by a shortening of the AP, and an increased contraction. Initial AP lengthening was associated with a more positive AP plateau which became more negative as the AP shortened. 4. There was a reversible reduction of Ca2+ current (ICa) during exposure to Strophanthidin. ICa changed reciprocally with contraction and with a similar time course. 5. Strophanthidin exposure caused a reduction of ICa at all activating voltages, suggesting that it resulted in a reduction of Ca2+ conductance with little change of its voltage dependence. 6. The role of an increase of intracellular calcium (Cai2+) was investigated by impaling myocytes with microelectrodes containing BAPTA 1,2-bis (2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid, a calcium chelator) to increase Cai2+ buffering. Strophanthidin still shortened the AP when BAPTA was present, suggesting that a rise of Cai2+ is not a major cause of AP shortening. 7. Although AP shortening was little affected, the decline of ICa with Strophanthidin was markedly reduced when BAPTA was present, suggesting that a rise of Cai2+ was the cause of the ICa decline with Strophanthidin. 8. When barium ions carried the current through Ca2+ channels, Strophanthidin did not reduce Ca2+ channel current, suggesting that this compound does not have a direct inhibitory effect on the channel. 9. The results suggest that Strophanthidin causes a reduction of ICa by increasing Cai2+, via the mechanism of Cai(2+)-dependent inactivation of ICa. The reduction of ICa at least partially explains the AP shortening and more negative plateau with Strophanthidin. 10. The shortening of the AP, more negative plateau and reduced ICa have negative inotropic effects which oppose the direct positive inotropic effect of Strophanthidin.
Strophanthidin-induced gain of Ca2+ occurs during diastole and not systole in guinea-pig ventricular myocytes
Pflugers Arch 1999 Apr;437(5):731-6.PMID:10087151DOI:10.1007/s004240050839.
We have investigated the effects of inhibiting the Na-K pump with Strophanthidin on the intracellular Ca2+ concentration ([Ca2+]i), sarcoplasmic reticulum (s.r.) Ca2+ content and membrane currents. s. r. Ca2+ content was measured by integrating the Na-Ca exchange current resulting from application of 10 mM caffeine. The application of Strophanthidin increased both diastolic and systolic [Ca2+]i. This was accompanied by an increase of s.r. Ca2+ content from a resting value of 17.9+/-1.5 micromol/l to 36.9+/-3.3 micromol/l (n=16) after 5 min. Systolic fluxes of Ca2+ into and out of the cell before and during Strophanthidin application were also measured. Ca2+ efflux (measured as the integral of the Na-Ca exchange tail current) rose steadily in the presence of Strophanthidin, while Ca2+ influx (the integral of the L-type Ca2+ current) was reduced. In spite of this, s.r. Ca2+ content rose substantially. In the presence of Cd2+ (100 microM), which inhibits the L-type Ca2+ current, Strophanthidin had negligible effects on current suggesting that Ca2+ influx via Na-Ca exchange during depolarization does not account for the increase of s.r. Ca2+ content. This suggests that changes of Ca2+ flux during systole are not responsible for the strophanthidin-induced increase of s.r. Ca2+. We conclude that the primary mechanism by which the cardiac cell gains Ca2+ when the Na-K pump is inhibited is by a net influx during diastole.
On the mechanism of the positive inotropy of low concentrations of Strophanthidin
J Pharmacol Exp Ther 1991 Oct;259(1):182-9.PMID:1920115doi
The hypothesis that low concentrations of Strophanthidin may decrease contractile force (and intracellular sodium activity, aiNa) under normal conditions but might increase force (while still decreasing aiNa) under conditions of increased Ca load was tested in sheep cardiac Purkinje fibers perfused in vitro. Strophanthidin was used at concentrations (7.5-25 nM, "low Strophanthidin") that decreased both force and aiNa in different preparations. A marked reduction in flow rate of Tyrode solution ("ischemia") increases aiNa and increases and eventually decreases force: during ischemia, low Strophanthidin decreases aiNa but increases force. High [Ca]o (16.2 mM) and norepinephrine (10 nM) increase force and decrease aiNa: in their presence, low Strophanthidin decreases aiNa further but increases force. Caffeine (4 mM) decreases force and increases aiNa, and low Strophanthidin increases force while having little effect on the increase of aiNa. In ventricular trabeculae, Strophanthidin decreases force under basal conditions but increases force during ischemia or Ca overload. Thus, Strophanthidin decreases force by lowering aiNa under normal conditions, but it increases force in spite (and perhaps because) of the decrease in aina under conditions of increased calcium load.
Determination of Strophanthidin in ingesta and plant material by LC-MS/MS
J Agric Food Chem 2004 Apr 21;52(8):2174-8.PMID:15080617DOI:10.1021/jf035443b.
An LC-MS/MS method was developed for the semiquantitative determination of Strophanthidin glycosides in ingesta from animals. Strophanthidin glycosides were simultaneously extracted and hydrolyzed to the Strophanthidin aglycone using aqueous methanolic hydrochloric acid and the extracts cleaned up using solid-phase extraction. Extracts were analyzed using reverse-phase HPLC coupled with positive ion electrospray mass spectrometry. Characteristic product ion spectra were produced by fragmentation of the [M + H](+) precursor ion for each analyte. Quantitation was performed using the internal standard method with digitoxigenin serving as the internal standard. The method detection limit was calculated to be 0.075 microg/g, and the limit of quantitation was calculated to be 0.24 microg/g for Strophanthidin in control rumen samples. This method was used in diagnostic investigations to confirm fatal Strophanthidin glycoside poisonings in horses.