Pregnenolone sulfate (sodium salt)
(Synonyms: 3β-Hydroxy-5-pregnen-20-one monosulfate sodium) 目录号 : GC44680A metabolite of pregnenolone
Cas No.:1852-38-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Pregnenolone sulfate is a metabolite of the natural steroid hormone pregnenolone . Pregnenolone sulfate modulates NMDA receptor responses to exogenously applied glutamate and stimulates transient receptor potential melastatin 3 (TRPM3).
| Cas No. | 1852-38-6 | SDF | |
| 别名 | 3β-Hydroxy-5-pregnen-20-one monosulfate sodium | ||
| Canonical SMILES | C[C@]12C(C[C@@H](OS([O-])(=O)=O)CC2)=CC[C@]3([H])[C@]1([H])CC[C@@]4(C)[C@@]3([H])CC[C@@H]4C(C)=O.[Na+] | ||
| 分子式 | C21H31O5S•Na | 分子量 | 418.5 |
| 溶解度 | 30 mg/ml in DMSO(Need ultrasonic); 2 mg/ml in Ethanol. | 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 | 2.3895 mL | 11.9474 mL | 23.8949 mL |
| 5 mM | 0.4779 mL | 2.3895 mL | 4.779 mL |
| 10 mM | 0.2389 mL | 1.1947 mL | 2.3895 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。
Pregnenolone sulfate enhances spontaneous glutamate release by inducing presynaptic Ca2+-induced Ca2+ release
Neuroscience 2010 Nov 24;171(1):106-16.PMID:20816925DOI:10.1016/j.neuroscience.2010.07.057.
Pregnenolone sulfate (PS) acts as an excitatory neuromodulator and has a variety of neuropharmacological actions, such as memory enhancement and convulsant effects. In the present study, we investigated the effect of PS on glutamatergic spontaneous excitatory postsynaptic currents (sEPSCs) in acutely isolated dentate gyrus (DG) hilar neurons by use of a conventional whole-cell patch-clamp technique. PS significantly increased sEPSC frequency in a concentration-dependent manner without affecting the current amplitude, suggesting that PS acts presynaptically to increase the probability of spontaneous glutamate release. However, known molecular targets of PS, such as α7 nicotinic ACh, NMDA, σ1 receptors and voltage-dependent Ca(2+) channels, were not responsible for the PS-induced increase in sEPSC frequency. In contrast, the PS-induced increase in sEPSC frequency was completely occluded in a Ca(2+)-free external solution, and was significantly reduced by either the depletion of presynaptic Ca(2+) stores or the blockade of ryanodine receptors, suggesting that PS elicits Ca(2+)-induced Ca(2+) release (CICR) within glutamatergic nerve terminals. In addition, the PS-induced increase in sEPSC frequency was completely occluded by transient receptor potential (TRP) channel blockers. These data suggest that PS increases spontaneous glutamate release onto acutely isolated hilar neurons via presynaptic CICR, which was triggered by the influx of Ca(2+) through presynaptic TRP channels. The PS-induced modulation of excitatory transmission onto hilar neurons could have a broad impact on the excitability of hilar neurons and affect the pathophysiological functions mediated by the hippocampus.
Inactivation of steroid sulfatase by an active site-directed inhibitor, estrone-3-O-sulfamate
Biochemistry 1995 Sep 12;34(36):11508-14.PMID:7547880DOI:10.1021/bi00036a025.
Steroid sulfatases are responsible for the hydrolysis of 3beta-hydroxy steroid sulfates, such as cholesterol and Pregnenolone sulfate, and have an important role in regulating the synthesis of estrogenic steroids, from estrone sulfate and dehydroepiandrosterone sulfate, in endocrine-dependent tumors. Although little is known about the mechanism by which the sulfate group is removed from a steroid nucleus, an active site-directed sulfatase inhibitor has been developed. This inhibitor, estrone-3-O-sulfamate (EMATE), was synthesized by treating the sodium salt of estrone with sulfamoyl chloride. This compound inhibited not only estrone sulfatase but also dehydroepiandrosterone sulfatase activity in placental microsomes and in intact MCF-7 breast cancer cells. Pretreatment of MCF-7 cells or placental microsomes with EMATE, followed by extensive washing or dialysis indicated irreversible inhibition. This was confirmed by showing that EMATE inhibited estrone sulfatase activity in placental microsomes in a time-, concentration-, and pH-dependent manner. The enzyme is protected from inactivation by estrone sulfate, which is also consistent with active site-directed inhibition. EMATE is proposed to inactivate estrone sulfatase by irreversible sulfamoylation of the enzyme. Maximum enzyme activity was detected at pH 8.6, and the maximum rate of enzyme inactivation by EMATE also occurred at this pH. The pKa values of the enzymatic reaction and pKa of inactivation were 7.2 and 9.8, providing evidence that two active site residues are being modified by EMATE. As the phenolic pKa of tyrosine (9.7) and the pKa of histidine will allow the roles that (6.8) are similar to the pKa values of inactivation, these amino acid residues may play a role in the catalytic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
The neurosteroid Pregnenolone sulfate excites medial vestibular nucleus neurons
Acta Otolaryngol Suppl 1998;533:22-5.PMID:9657306doi
To examine the relationship between neurosteroids and vertigo we performed electrophysiological studies to determine whether Pregnenolone sulfate (PS) affects the activity of medial vestibular nucleus (MVN) neurons in alpha-chloralose-anesthetized cats. Single neuronal activities in the MVN were recorded extracellularly using a glass-insulated silver wire microelectrode attached along a seven-barreled micropipette. 3 mM PS, 1 M glutamate and 3 mM NaCl were applied microiontophoretically in the immediate vicinity of the target neurons. The effects of these drugs were then examined on type I and type II neurons, identified by their responses to horizontal and sinusoidal rotations. The iontophoretic application of PS dose-dependently increased the spontaneous firing of both type I and type II neurons. The larger increase in firing was observed in type I neurons as compared with type II neurons following the PS application. These results suggest that PS excites types I and II neurons differentially, presumably resulting in a disturbance of harmony of the vestibulo-ocular reflex with ensuing development of vertigo.