Dehydroepiandrosterone (DHEA)
(Synonyms: 脱氢表雄酮; Prasterone; Dehydroisoandrosterone; Dehydroepiandrosterone) 目录号 : GC11070
An endogenous steroid hormone
Cas No.:53-43-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
HCC1 cell line |
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Preparation Method |
Transferred cells to serum-free dehydroepiandrosterone (DHEA) containing either 0.1% ethanol which was added to all control cultures or 10-12-10-6 M DHEA. The cell culture supernatant was harvested after 72 h. |
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Reaction Conditions |
10-12-10-6 M for 72 hours |
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Applications |
Co-treatment with DEX (10-7 M)/ANDI (10-7 M) or DEX (10-7 M)/DHEA (10-7 M) reversed the increase in RANKL mRNA expression |
| Animal experiment [2]: | |
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Animal models |
female BALB/c mice |
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Preparation Method |
Effects of treatment with dehydroepiandrosterone (DHEA) were assessed on either ovaries with functional corpora lutea (CL) or regressing CL by two s.c. injections of 60 mg DHEA/kg body weight (DHEA group), 24 h apart on days 3 and 4 after ovulation, followed by decapitation on day 5 (functional CL) or on day 7 and 8, followed by decapitation on day 9 (regressing CL). |
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Dosage form |
s.c., 60 mg/kg |
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Applications |
In mice with functional CL (day 5), the hyperandrogenization with dehydroepiandrosterone (DHEA) decreased both serum P and estradiol (E2) levels when compared to controls |
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References: [1]: Harding G, Mak YT, Evans B, Cheung J, MacDonald D, Hampson G: The effects of dexamethasone and dehydroepiandrosterone (DHEA) on cytokines and receptor expression in a human osteoblastic cell line: potential steroid-sparing role of DHEA. Cytokine. 2006, 36: 57-68. 10.1016/j.cyto.2006.10.012. |
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Dehydroepiandrosterone (DHEA) and its sulfate ester, DHEAS, together represent the most abundant steroid hormones in the human body [1].
Dehydroepiandrosterone (DHEA) (10-8 and 10-6 M) or DHEAS pretreated rat cerebral cortical cultures was increased neuronal survival when the cultures subjected to anoxia for 2 h [2]. When rat cerebral cortical cultures were subjected to anoxia for 2 h in an anaerobic chamber and pretreated with dehydroepiandrosterone (DHEA) (10-8 and 10-6 M) or DHEAS (10-6 M), there was increased neuronal survival. Using cultured neural precursors from rat embryonic forebrains, dehydroepiandrosterone (DHEA) (50 and 100 nM) activated the serine-threonine protein kinase Akt, which is widely implicated in cell survival signaling [3].
Dehydroepiandrosterone (DHEA) treating had better locomotor recovery on CD-1 female mice, after contusive spinal cord injury (SCI), and also left-right coordination, and fine motor control than control animals [4]. Mice treated with dehydroepiandrosterone (DHEA) also had significantly more white matter spared at the epicenter of the injury and reduced area of reactive gliosis surrounding the lesion. Dehydroepiandrosterone (DHEA) treatment was intensive and consisted of three different modes of administration: a DHEA Matrigel patch (10-10 M) applied to the spinal cord before closure of the wound, followed by 12 days of i.p. injections of saline containing Dehydroepiandrosterone (DHEA) (10-6 M or 0.02 mg/kg/day) after SCI, and Dehydroepiandrosterone (DHEA) (10-6 M) in the drinking water for 42 days [4].
References:
[1]. Rice SP, Zhang L, Grennan-Jones F, Agarwal N, Lewis MD, Rees DA, Ludgate M: Dehydroepiandrosterone (DHEA) treatment in vitro inhibits adipogenesis in human omental but not subcutaneous adipose tissue. Mol Cell Endocrinol 2010, 320: 51-57. 10.1016/j.mce.2010.02.017
[2]. C.E. Marx, L.F. Jarskog, J.M. Lauder, J.H. Gilmore, J.A. Lieberman, A.L. Morrow. Neurosteroid modulation of embryonic neuronal survival in vitro following anoxia. Brain Res., 871 (2000), pp. 104-112
[3]. L. Zhang, B. Li, W. Ma, J.L. Barker, Y.H. Chang, W. Zhao, D.R. Rubinow. Dehydroepiandrosterone (DHEA) and its sulfated derivative (DHEAS) regulate apoptosis during neurogenesis by triggering the Akt signaling pathway in opposing ways. Brain Res. Mol. Brain Res., 98 (2002), pp. 58-66
[4]. C. Fiore, D.M. Inman, S. Hirose, L.J. Noble, T. Igarashi, N.A. Compagnone. Treatment with the neurosteroid dehydroepiandrosterone promotes recovery of motor behavior after moderate contusive spinal cord injury in the mouse. J. Neurosci. Res., 75 (2004), pp. 391-400
脱氢表雄酮 (DHEA) 及其硫酸酯 DHEAS 共同代表了人体内最丰富的类固醇激素[1]。
脱氢表雄酮 (DHEA)（10- 8 和 10-6 M) 或 DHEAS 预处理的大鼠大脑皮层培养物在缺氧 2 小时后神经元存活率增加 [2]。当大鼠大脑皮质培养物在厌氧室中缺氧 2 小时并用脱氢表雄酮 (DHEA)（10-8 和 10-6 M）或 DHEAS（10-6 M）预处理时，神经元存活率增加。使用来自大鼠胚胎前脑的培养神经前体，脱氢表雄酮 (DHEA)（50 和 100 nM）激活丝氨酸-苏氨酸蛋白激酶 Akt，后者广泛参与细胞存活信号转导[3]。
在挫伤性脊髓损伤 (SCI) 后，脱氢表雄酮 (DHEA) 治疗对 CD-1 雌性小鼠的运动恢复、左右协调和精细运动控制均优于对照动物[4]< /sup>。用脱氢表雄酮 (DHEA) 治疗的小鼠在损伤中心也有明显更多的白质，并且损伤周围的反应性神经胶质增生区域减少。脱氢表雄酮 (DHEA) 治疗是强化治疗，由三种不同的给药方式组成:在伤口闭合前将 DHEA Matrigel 贴剂 (10-10 M) 应用于脊髓，然后进行 12 天的腹膜内注射。脊髓损伤后注射含脱氢表雄酮（DHEA）（10-6 M 或 0.02 mg/kg/天）的生理盐水，并在饮用水中注射脱氢表雄酮（DHEA）（10-6 M）42天[4].
| Cas No. | 53-43-0 | SDF | |
| 别名 | 脱氢表雄酮; Prasterone; Dehydroisoandrosterone; Dehydroepiandrosterone | ||
| 化学名 | (3S,8R,9S,10R,13S,14S)-3-hydroxy-10,13-dimethyl-1,2,3,4,7,8,9,11,12,14,15,16-dodecahydrocyclopenta[a]phenanthren-17-one | ||
| Canonical SMILES | CC12CCC3C(C1CCC2=O)CC=C4C3(CCC(C4)O)C | ||
| 分子式 | C19H28O2 | 分子量 | 288.42 |
| 溶解度 | ≥ 13.7 mg/mL in DMSO, ≥ 58.6 mg/mL in ETOH | 储存条件 | Store at RT |
| 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 | 3.4672 mL | 17.3358 mL | 34.6717 mL |
| 5 mM | 0.6934 mL | 3.4672 mL | 6.9343 mL |
| 10 mM | 0.3467 mL | 1.7336 mL | 3.4672 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。
Dehydroepiandrosterone (DHEA): hypes and hopes
Dehydroepiandrosterone (DHEA) and its sulfated form dehydroepiandrosterone sulfate (DHEAS) are the most abundant circulating steroid hormones in humans. In animal studies, their low levels have been associated with age-related involuntary changes, including reduced lifespan. Extrapolation of animal data to humans turned DHEA into a 'superhormone' and an 'anti-aging' panacea. It has been aggressively marketed and sold in large quantities as a dietary supplement. Recent double-blind, placebo-controlled human studies provided evidence to support some of these claims. In the elderly, DHEA exerts an immunomodulatory action, increasing the number of monocytes, T cells expressing T-cell receptor gamma/delta (TCRγδ) and natural killer (NK) cells. It improves physical and psychological well-being, muscle strength and bone density, and reduces body fat and age-related skin atrophy stimulating procollagen/sebum production. In adrenal insufficiency, DHEA restores DHEA/DHEAS and androstenedione levels, reduces total cholesterol, improves well-being, sexual satisfaction and insulin sensitivity, and prevents loss of bone mineral density. Normal levels of CD4+CD25(hi) and FoxP3 (forkhead box P3) are restored. In systemic lupus erythematosus, DHEA is steroid-sparing. In an unblinded study, it induced remission in the majority of patients with inflammatory bowel disease. DHEA modulates cardiovascular signalling pathways and exerts an anti-inflammatory, vasorelaxant and anti-remodelling effect. Its low levels correlate with increased cardiovascular disease and all-cause mortality. DHEA/DHEAS appear protective in asthma and allergy. It attenuates T helper 2 allergic inflammation, and reduces eosinophilia and airway hyperreactivity. Low levels of DHEAS accompany adrenal suppression. It could be used to screen for the side effects of steroids. In women, DHEA improves sexual satisfaction, fertility and age-related vaginal atrophy. Many factors are responsible for the inconsistent/negative results of some studies. Overreliance on animal models (DHEA is essentially a human molecule), different dosing protocols with non-pharmacological doses often unachievable in humans, rapid metabolism of DHEA, co-morbidities and organ-specific differences render data interpretation difficult. Nevertheless, a growing body of evidence supports the notion that DHEA is not just an overrated dietary supplement but a useful drug for some, but not all, human diseases. Large-scale randomised controlled trials are needed to fine-tune the indications and optimal dosing protocols before DHEA enters routine clinical practice.
Effect of Dehydroepiandrosterone (DHEA) on Diabetes Mellitus and Obesity
Type 2 diabetes is a metabolic disorder that is characterized by an impaired capacity to secrete insulin, insulin resistance, or both. Dehydroepiandrosterone (DHEA), a steroid hormone produced by the adrenal cortex, has been reported to have beneficial effects on diabetes mellitus and obesity in animal models. DHEA and DHEA-sulfate (DHEA-S) have been reported to increase not only insulin secretion of the pancreas but also insulin sensitivity of the liver, adipose tissue, and muscle. We investigated the effects of DHEA on glucose metabolism in animal models and reported decrease of liver gluconeogenesis. Recently, we reported the effect of DHEA on the liver and muscle by using insulin-stimulated insulin receptor substrate 1 and 2 (IRS1 and IRS2)-deficient mice. DHEA increased Akt phosphorylation in the liver of C57BL6 IRS1- and IRS2-deficient mice fed with a high-fat diet (HFD), which suggests that the increase in DHEA-induced Akt signaling is sufficient in the presence of IRS1 or IRS2. In addition, other studies have also reported the effect of DHEA on diabetes mellitus in the liver, muscle, adipose tissue, and pancreatic β-cell and its effect on obesity in animal models. A meta-analysis in elderly men and women has found that DHEA supplementation has no effects on blood glucose levels. However, DHEA supplementation to patients with type 2 diabetes has not been fully elucidated. Therefore, further studies are needed to provide greater insight into the effect of DHEA on diabetes and obesity in animal and human models.
Dehydroepiandrosterone (DHEA) supplementation and IVF outcome in poor responders
Ovarian stimulation of poor ovarian responders still remains a challenging issue. The incidence of poor responders among infertile women is reported in 9-24% IVF cycles and is associated with very low clinical pregnancy rates. Different treatments have been reported in the literature in an attempt to identify the best stimulation protocol for those patients. Administration of dehydroepiandrosterone acetate (DHEA) was suggested as a promising treatment. It is well known that androgens can influence ovarian follicular growth, augment steroidogenesis, promote follicular recruitment and increase the number of primary and pre-antral follicles. The purpose of this review is to evaluate the effect of DHEA supplementation on women with diminished ovarian reserve. Because of the uncertainty of published data, we suggest that well-designed multicentre RCTs are required to provide more insight on the effectiveness of DHEA. The absence of significant side effects should not be considered as an argument to support DHEA treatment.
[Dehydroepiandrosterone(DHEA)and bone metabolism]
Dehydroepiandrosterone(DHEA), an adrenal androgen, has attracted much attention as an anti-aging hormone as well as a marker for senescence because of its unique change along with aging. DHEA is reported to have beneficial effects such as anti-diabetes, anti-obesity, and anti-atherosclerosis. It is also shown that DHEA has anti-osteoporosis effects to increase bone mineral density in randomized controlled trials(RCTs). As osteoblasts express aromatase which will convert androgen to estrogen, DHEA may act protectively against osteoporosis through its metabolites. Because there is no report on fracture risk by DHEA administration, further studies are required to clarify DHEA effects on human bone metabolism.