DHEA

53-43-0

C19H28O2

DMSO : 50 mg/mL (173.36 mM; Need ultrasonic)

Others; Metabolic Enzyme/Protease

DHEA (Prasterone) is one of the most abundant steroid hormones. DHEA (Prasterone) mediates its action via multiple signaling pathways involving specific membrane receptors and via transformation into androgen and estrogen derivatives (e.g., androgens, estrogens, 7alpha and 7beta DHEA, and 7alpha and 7beta epiandrosterone derivatives) acting through their specific receptors. IC50 & Target: Androgen receptor^[1] In Vitro: DHEA (Prasterone) is an effective antiapoptotic factor, reversing the serum deprivation-induced apoptosis in prostate cancer cells (DU145 and LNCaP cell lines) as well as in colon cancer cells (Caco2 cell line). DHEA (Prasterone) significantly reduces serum deprivation-induced apoptosis in all 3 cancer cell types, quantitated with the APOPercentage assay (apoptosis is reduced from 0.587+/-0.053 to 0.142+/-0.0016 or 0.059+/-0.002 after treatment for 12 hours with DHEA or NGF, respectively; n=3, P<0.01), and by flow cytometry analysis (FACS) for DU145 cells. The antiapoptotic effect of DHEA is dose dependent with an EC50 at nanomolar concentrations (EC₅₀: 11.2+/-3.6 nM and 12.4+/-2.2 nM in DU145 and Caco2 cells, respectively)^[1]. DHEA (Prasterone) is the principal sex steroid precursor in humans and can be converted directly to androgens. DHEA (Prasterone) (>=1 uM) causes a dose-dependent inhibition of Chub-S7 proliferation, as assessed by thymidine incorporation assays. DHEA (Prasterone) treatment inhibits expression of the key glucocorticoid-regulating genes H6PDH (>=100 nM) and HSD11B1 (>=1 uM) in differentiating preadipocytes in a dose-dependent manner. In keeping with this finding, DHEA (Prasterone) treatment (>=1 uM) results in a marked reduction in 11beta-HSD1 oxoreductase activity (>=1 uM) and a concurrent increase in dehydrogenase activity at the highest DHEA dose used (25 uM DHEA) in differentiated adipocytes^[2]. In Vivo: DHEA (Prasterone) in the diet (0.45 % w/w) of male B6 mice (groups of five mice) treated for 8 weeks led to significant decreases in body temperature compared with mice fed the control AIN-76A diet. A similar comparison indicated that control and pair-fed mice are also significantly different. Animals fed DHEA (Prasterone) have significantly lower temperatures than mice fed the control diet 26/29 times tested; mice pair fed to those on the DHEA (Prasterone) diet are less affected, with 8/29 values significantly lower than in mice fed AIN-76A ad libitum. The temperatures of mice fed DHEA (Prasterone) or pair fed to DHEA (Prasterone) are significantly different 21/29 times tested. Body weights are significantly greater in mice fed the control diet than in mice fed DHEA or pair fed to DHEA (Prasterone). Food intake (grams per day) from cages are averaged for each week (n=7), except for Week 9 (n=3). The amount of food intake is significantly decreased in mice fed DHEA (Prasterone). By design, mice pair fed to DHEA (Prasterone) ate about the same amount. Thus, it appears that DHEA (Prasterone) reduces body temperature by food restriction and by a separate mechanism^[3].