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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.