Protective effects of dehydroepiandrosterone on atherosclerosis in ovariectomized rabbits via alleviating inflammatory injury in endothelial cells

A pharmacological mouse model suggests a novel risk pathway for postpartum psychosis

“…Moreover, whilst 667-COUMATE is an effective inhibitor of STS, it may have off-target effects, notably on carbonic anhydrase II (Ho et al, 2003); these off-target effects have no gross effects on maternal health, but their contribution to the more subtle changes in drug-treated mice is difficult to quantify. In support of steroid sulfatase inhibition-mediated effects on the gene expression differences reported here, DHEA influences Ctgf / Ccn2 (Zhang et al, 2013) and Ccl2 (or MCP-1 )(Wang et al, 2011) expression and secretion in females.…”

A Review of Age-Related Dehydroepiandrosterone Decline and Its Association with Well-Known Geriatric Syndromes: Is Treatment Beneficial?

“…[93][94][95][96] Current opinion consensus supports a lipid profile independent mechanism mediating the anti-atherosclerotic effects of DHEA, 18,[93][94][95] partly through transformation to estrogens and testosterone. 97 The previously described anti-inflammatory effects of DHEA, 18,95 as well as direct stimulation of eNOS could also participate. 17,18 Indeed, low DHEAS predicted incident ischemic heart disease in a group of men in a 9-year follow-up study, independently from classic cardiovascular risk factors.…”

DHEA promotes osteoblast differentiation by regulating the expression of osteoblast-related genes and Foxp3⁺ regulatory T cells

“…The level of dehydroepiandrosterone (DHEA) in postmenopausal women is lower than that in fertile women, which suggests the potential clinical benefit of DHEA as treatment for postmenopausal osteoporosis (PMO) (1). Treatment of postmenopausal osteoporosis is mainly hormone replacement therapy, but this therapy is often accompanied by adverse reactions, limiting its use (2,3).…”