product name Related androgen products
Description: Dehydroepiandrosterone is an important endogenous steroid hormone, which functions as an androgen receptor antagonist and an estrogen receptor agonist. DHEA is acts 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. DHEA significantly increased neural stem cells growth when grew with leukemia inhibitory factor and EGF.
References: Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1852-7; Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4678-83.
288.43
Formula
C19H28O2
CAS No.
53-43-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 57 mg/mL (197.6 mM)
Water: <1 mg/mL
Ethanol: 57 mg/mL (197.6 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19394780
| In Vitro |
In vitro activity: Dehydroepiandrosterone reversibly blocks GABA-induced currents, behaving as an allosteric antagonist of the GABAA receptor in cultured neurons from ventral mesencephalon. Dehydroepiandrosterone (DHEA) protects primary hippocampal cultures from embryonic day 18 (E18) embryos against NMDA-induced toxicity, DHEAS also reduces NMDA-induced toxicity. DHEA (100 nM) protects cultured neurons against the neurotoxic actions of either AMPA (25 mM) or kainic acid (1 mM) as well. Dehydroepiandrosterone (DHEA) increases the length of neurites containing the axonal marker Tau-1 in primary cultures of mouse embryonic neocortical neurons, and the incidence of varicosities and basket-like process formations in a dose-dependent fashion. Dehydroepiandrosterone (DHEA) rapidly increases free intracellular calcium via activation of N-methyl-D-aspartate (NMDA) receptors. Dehydroepiandrosterone with H874Y stimulates a 3- to 8-fold greater response than with wild type AR and at 100 nM the response is similar with the LNCaP mutant in the androgen-dependent human prostate cancer xenograft CWR22 and LNCaP cells. Kinase Assay: Cell Assay: Treatment of T. crassiceps with DHEA decreasd reproduction, motility and viability in a dose- and time-dependent fashion. 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. |
|---|---|
| In Vivo | Dehydroepiandrosterone increases the number of newly formed cells in the dentate gyrus of the hippocampus of adult male rats, and also antagonizes the suppressive of corticosterone (40 mg/kg body weight daily for 5 days). Dehydroepiandrosterone by itself increases the number of newly formed neurons, but only if treatment is continued throughout the period of survival. |
| Animal model | Ovarian cortical autograft (‘normograft’) model; or rats model |
| Formulation & Dosage | DHEA single rod implants (length 5 cm, diameter 3.35 mm); s.c administration. |
| References | Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1852-7; Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4678-83. |
Related Posts
product name Related androgen products
Description: Dehydroepiandrosterone is an important endogenous steroid hormone, which functions as an androgen receptor antagonist and an estrogen receptor agonist. DHEA is acts 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. DHEA significantly increased neural stem cells growth when grew with leukemia inhibitory factor and EGF.
References: Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1852-7; Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4678-83.
288.43
Formula
C19H28O2
CAS No.
53-43-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 57 mg/mL (197.6 mM)
Water: <1 mg/mL
Ethanol: 57 mg/mL (197.6 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19394780
| In Vitro |
In vitro activity: Dehydroepiandrosterone reversibly blocks GABA-induced currents, behaving as an allosteric antagonist of the GABAA receptor in cultured neurons from ventral mesencephalon. Dehydroepiandrosterone (DHEA) protects primary hippocampal cultures from embryonic day 18 (E18) embryos against NMDA-induced toxicity, DHEAS also reduces NMDA-induced toxicity. DHEA (100 nM) protects cultured neurons against the neurotoxic actions of either AMPA (25 mM) or kainic acid (1 mM) as well. Dehydroepiandrosterone (DHEA) increases the length of neurites containing the axonal marker Tau-1 in primary cultures of mouse embryonic neocortical neurons, and the incidence of varicosities and basket-like process formations in a dose-dependent fashion. Dehydroepiandrosterone (DHEA) rapidly increases free intracellular calcium via activation of N-methyl-D-aspartate (NMDA) receptors. Dehydroepiandrosterone with H874Y stimulates a 3- to 8-fold greater response than with wild type AR and at 100 nM the response is similar with the LNCaP mutant in the androgen-dependent human prostate cancer xenograft CWR22 and LNCaP cells. Kinase Assay: Cell Assay: Treatment of T. crassiceps with DHEA decreasd reproduction, motility and viability in a dose- and time-dependent fashion. 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. |
|---|---|
| In Vivo | Dehydroepiandrosterone increases the number of newly formed cells in the dentate gyrus of the hippocampus of adult male rats, and also antagonizes the suppressive of corticosterone (40 mg/kg body weight daily for 5 days). Dehydroepiandrosterone by itself increases the number of newly formed neurons, but only if treatment is continued throughout the period of survival. |
| Animal model | Ovarian cortical autograft (‘normograft’) model; or rats model |
| Formulation & Dosage | DHEA single rod implants (length 5 cm, diameter 3.35 mm); s.c administration. |
| References | Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1852-7; Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4678-83. |