Background Dehydroepiandrosterone (DHEA) is widely known for its beneficial effect on postmenopausal osteoporosis,although the underlying mechanisms remain mainly unclear.In this study,we tried to determine the activation of mitogen-activated protein kinase signal pathways during DHEA treatment and the indirect role of osteoblasts (OBs) on osteoclasts under the DHEA treatment of postmenopausal osteoporosis.@@Methods Primary human OBs and osteoclast-like cells were cultured and,we pretreated OBs with or without U0126 (a highly selective inhibitor of both MEK1 and MEK2).The OBs were treated with DHEA.We then tested the effects of DHEA on human osteoblastic viability,osteoprotegerin production and the expression of phosphor-ERK1/2 (extracellular signal-regulated kinase).In the presence or absence of OBs,the function of osteoclastic resorption upon DHEA treatment was calculated.@@Results DHEA promoted the human osteoblastic proliferation and inhibited the osteoblastic apoptosis within the concentration range of 108-10-6 mol/L (P