Dehydroepiandrosterone (DHEA) [53-43-0]
Referencia B1375-1ml
embalaje : 10mM(in1mLDMSO)
Marca : APExBIO Technology
Contact local distributor :
Teléfono : +1 850 650 7790
Dehydroepiandrosterone (DHEA)
Dehydroepiandrosterone (DHEA) is an important endogenous steroid hormone [1].
DHEA is an important endogenous steroid hormone and functions as a metabolic intermediate in the biosynthesis of estrogen and androgen. Also, DHEA has a variety of potential biological effects by binding to nuclear and cell surface receptors and acts as a neurosteroid.
In human neural stem cells derived from the fetal cortex, DHEA significantly increased cells growth when grew with leukemia inhibitory factor (LIF) and epidermal growth factor (EGF). Also, DHEA increased neuronal production by 29%. In glial fibrillary acidic protein-positive cells, DHEA significantly increased cells growth, the mRNA and protein of acidic protein [2]. In rat chromaffin cells and pheochromocytoma PC12 cell line, DHEA protected cells against serum deprivation-induced apoptosis with EC50 value of 1.8 nM. DHEA increased the expression of NF-κB and cAMP response element-binding protein, upstream effectors of antiapoptotic Bcl-2 protein. DHEA also activated PKC ɑ/β, a posttranslational activator of Bcl-2 [3].
In male Lister hooded rats, s.c. pellets of DHEA protected hippocampal CA1/2 neurons against N-methyl-D-aspartic acid (NMDA) (5 or 10 nM) [1].
References:
[1]. Kimonides VG, Khatibi NH, Svendsen CN, et al. Dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEAS) protect hippocampal neurons against excitatory amino acid-induced neurotoxicity. Proc Natl Acad Sci U S A, 1998, 95(4): 1852-1857.
[2]. Suzuki M, Wright LS, Marwah P, et al. Mitotic and neurogenic effects of dehydroepiandrosterone (DHEA) on human neural stem cell cultures derived from the fetal cortex. Proc Natl Acad Sci U S A, 2004, 101(9): 3202-3207.
[3]. Charalampopoulos I, Tsatsanis C, Dermitzaki E, et al. Dehydroepiandrosterone and allopregnanolone protect sympathoadrenal medulla cells against apoptosis via antiapoptotic Bcl-2 proteins. Proc Natl Acad Sci U S A, 2004, 101(21): 8209-8214.
- 1. Shanmeizi Zhao, Rujun Ma, et al. "ZDHHC17 participates in the pathogenesis of polycystic ovary syndrome by affecting androgen conversion to estrogen in granulosa cells." Mol Cell Endocrinol. 2023 Dec 1:578:112076. PMID: 37769867
- 2. Yanjun Liu, Yang Wang, et al. "Diane-35 and Metformin Induce Autophagy and Apoptosis in Polycystic Ovary Syndrome Women with Early-Stage Endometrial Carcinoma." Genes (Basel). 2022 Jan 12;13(1):131. PMID: 35052471
- 3. Fanru Zhou, Yufan Song, et al. "Si-Wu-Tang facilitates ovarian function through improving ovarian microenvironment and angiogenesis in a mouse model of premature ovarian failure." J Ethnopharmacol. 2021 Nov 15;280:114431. PMID: 34293457
- 4. Yan Lu, E Wang, et al. "Obesity-induced excess of 17-hydroxyprogesterone promotes hyperglycemia through activation of glucocorticoid receptor." J Clin Invest. 2020 Jul 1;130(7):3791-3804. PMID: 32510471
| Physical Appearance | A solid |
| Storage | Store at -20°C |
| M.Wt | 288.42 |
| Cas No. | 53-43-0 |
| Formula | C19H28O2 |
| Solubility | insoluble in H2O; ≥13.7 mg/mL in DMSO; ≥58.6 mg/mL in ETOH |
| Chemical Name | (3S,8R,9S,10R,13S,14S)-3-hydroxy-10,13-dimethyl-1,2,3,4,7,8,9,11,12,14,15,16-dodecahydrocyclopentaamphenanthren-17-one |
| SDF | Download SDF |
| Canonical SMILES | O=C1[C@]2(C)[C@@H](CC1)[C@H]3[C@H](CC2)[C@](CC[C@@H]4O)(C)C(C4)=CC3 |
| Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
| General tips | We do not recommend long-term storage for the solution, please use it up soon. |
| Cell experiment: | |
| Cell lines | Cysticerci; hippocampal |
| Preparation method | This compound is soluble in DMSO and in ethanol. General tips for obtaining a higher concentration: Please warm the tube at 37℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
| Reacting condition | 1.7, 3.5, 7 μM for 1-10 days; or 10–100 nM for 6–8 h |
| Applications | Treatment of T. crassiceps with DHEA decreasd reproduction, motility and viability in a dose- and time-dependent fashion [1]. Moreover, Pre-treatment with DHEA (10–100 nM for 6–8 h) protected hippocampal neurons against excitatory amino acid (0.1, 1, 10, and 50 mM)-induced neurotoxicity in vitro [2]. |
| Animal experiment: | |
| Animal models | Ovarian cortical autograft (‘normograft’) model; or rats model |
| Dosage form | DHEA single rod implants (length 5 cm, diameter 3.35 mm), subcutaneous administration for 10 weeks. |
| Applications | DHEA promoted granulosa cell proliferation and increased the follicular anti-Mullerian hormone (AMH) expression at the preantral and early antral follicle stages [3]. Moreover, DHEA protected hippocampal neurons against N-methyl-D-aspartic acid (NMDA)-induced neurotoxicity in vivo [2]. |
| Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| References: 1. Vargas-Villavicencio, J. A., Larralde, C. and Morales-Montor, J. (2008) Treatment with dehydroepiandrosterone in vivo and in vitro inhibits reproduction, growth and viability of Taenia crassiceps metacestodes. Int J Parasitol. 38, 775-781 2. Kimonides, V. G., Khatibi, N. H., Svendsen, C. N., Sofroniew, M. V. and Herbert, J. (1998) Dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEAS) protect hippocampal neurons against excitatory amino acid-induced neurotoxicity. Proc Natl Acad Sci U S A. 95, 1852-1857 3. Narkwichean, A., Jayaprakasan, K., Maalouf, W. E., Hernandez-Medrano, J. H., Pincott-Allen, C. and Campbell, B. K. (2014) Effects of dehydroepiandrosterone on in vivo ovine follicular development. Hum Reprod. 29, 146-154 | |