3β-Hydroxy-androst-5-ene-17-one/DHEA/17-Hormoforin/3-β-hydroxyandrost-5-en-17-one/3b-hydroxy-Androst-5-en-17-one/(3b)-3-Hydroxyandrost-5-en-17-one/3β-hydroxy-androst-5-en-17-one/(3β)-3-hydroxy-Androst-5-en-17-one/D5-Androsten-3b-ol-17-one/(3β)-3-Hydroxyandrost-5-en-17-one/Psicosterone/Prasterone/trans-Dehydroandrosterone/3b-Hydroxyandrost-5-ene-17-one/Androst-5-en-17-one, 3β-hydroxy-/Androst-5-en-17-one, 3-hydroxy-, (3β)-/3b-Hydroxyandrost-5-en-17-one/Prestara/3β-Hydroxy-5-androsten-17-one/Intrarosa/Deandros/dehydroisoandrosterone/(3β)-3-Hydroxyandrost-5-ene-17-one/Androst-5-ene-3b-ol-17-one/Androst-5-ene-3β-ol-17-one/5-Androsten-3β-ol-17-one/Dehydro-epi-androsterone/17-Chetovis/Dehydroepiandrosterone/didehydroepiandrosterone/3β-Hydroxyandrost-5-ene-17-one/D5-Androsten-3β-ol-17-one/Diandrone/Astenile/3β-Hydroxyandrost-5-en-17-one/Diandron
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provides coniferyl ferulate(CAS#:53-43-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Despite an increased understanding of the pathogenesis of osteoarthritis (OA) and the availability of a number of drugs designed to ameliorate its symptoms, a successful disease-modifying therapy remains elusive. Recent lines of evidence suggest that dehydroepiandrosterone (DHEA), a 19-carbon steroid hormone classified as an adrenal androgen, exerts a chondroprotective effect in OA patients, and it has been proven to be an effective DMOAD candidate that slows OA progression. However, the exact mechanisms underlying its anti-OA effect is largely unknown. This review summarizes emerging observations from studies of cell biology, preclinical animal studies, and preliminary clinical trials and describes the findings of investigations on this topic to develop an initial blueprint of the mechanisms by which DHEA slows OA progression. Presently, studies on DMOADs are increasing in importance but have met limited success. Encouragingly, the current data on DHEA are promising and may prove that DHEA-based treatment is efficacious for preventing and slowing human OA progression.
Articular cartilage; Dehydroepiandrosterone; Inflammation; Osteoarthritis; Signaling pathways.
Dehydroepiandrosterone and Experimental Osteoarthritis
Kai Huang 1 , Li-Dong Wu 2 , Jia-Peng Bao 2
Steroid hormones are important regulators of brain development, physiological function, and behavior. Among them, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulfate (DHEAS) also do modulate emotional processing and may have mood enhancement effects. This chapter reviews the studies that bear relation to DHEA and DHEAS [DHEA(S)] and brain emotional processing and behavior. A brief introduction to the mechanisms of action and variations of DHEA(S) levels throughout life has also been forward in this chapter. Higher DHEA(S) levels may reduce activity in brain regions involved in the generation of negative emotions and modulate activity in regions involved in regulatory processes. At the electrophysiological level, higher DHEA-to-cortisol and DHEAS-to-DHEA ratios were related to shorter P300 latencies and shorter P300 amplitudes during the processing of negative stimuli, suggesting less interference of negative stimuli with the task and less processing of the negative information, which in turn may suggest a protective mechanism against negative information overload. Present knowledge indicates that DHEA(S) may play a role in cortical development and plasticity, protecting against negative affect and depression, and at the same time enhancing attention and overall working memory, possibly at the cost of a reduction in emotional processing, emotional memory, and social understanding.
Attention; Cortisol; Dehydroepiandrosterone; Dehydroepiandrosterone-sulfate; Depression; Emotion processing; Emotional memory; Event-related potentials; Neuroimaging
Dehydroepiandrosterone and Dehydroepiandrosterone-Sulfate and Emotional Processing
Sonia do Vale 1 , Carles Escera 2
The dehydroepiandrosterone and its metabolite, dehydroepiandrosterone sulfate, have been for a long while at the center of interest for endocrinologists and cardiologists. Consolidated data show that the dehydroepiandrosterone and the dehydroepiandrosterone sulfate present protective actions on the cardiovascular system. These actions are accomplished directly through target tissues such as endothelial cells, smooth muscle cells, and cardiomyocytes. At this level, they are able to activate a complex group of receptor, not completely identified, which modulate important functions such as vasodilation, antiinflammation, and antithrombosis. These data support the hypothesis that dehydroepiandrosterone could be used as drug for primary prevention of cardiovascular disease especially during aging and potentially also in addition of the common therapeutic strategy for the treatment and prevention of cardiovascular disease recurrence. In this publication, the effects of dehydroepiandrosterone and dehydroepiandrosterone sulfate on the cardiovascular system have been elucidated, starting with an analysis of the molecular action at target organ levels. In the second part, we evaluated the clinical effects of this administration, considering ultimately possible implications in introducing this hormone into clinical practice.
Aging; Cardiovascular disease; Cardiovascular system; Dehydroepiandrosterone; Dehydroepiandrosterone sulfate.
Dehydroepiandrosterone and Cardiovascular Disease
P Mannella 1 , T Simoncini 1 , M Caretto 1 , A R Genazzani 2
DHEA is one of the most abundant steroid hormones. DHEA mediates its action via multiple signaling pathways involving specific membrane receptors and via transformation into androgen and estrogen derivatives (e.g., androgens, estrogens, 7α and 7β DHEA, and 7α and 7β epiandrosterone derivatives) acting through their specific receptors.