ObjectiveExploring the role of hypoxia-induceibal factor-1 (HIF-1) signaling pathway in postmenstrual osteoporosis (PMOP) and how to play a role in PMOP. MethodsSixty C57BL/6J female mouse were randomly divided into 4 groups: sham-operation group (A group), ovariectomized PMOP group (B group), HIF-1 alpha inhibitor 2-methoxy estradiol (2ME2) treatment group(D group) and solvent control group(C group), 15 mice in each group. There months after modeling, the metabolism product of mouse bone tissue including serum propeptide of typeⅠ procollagen (PINP), C-terminal telopeptide-Ⅰ (CTX-1) and serum estrogen were quantified by enzyme-linked immunosorbent assay (ELISA). Changes of bone structure were observed on HE stained tissue sections. Regulation products of HIF-1 signaling pathway including HIF-1α, HIF-1β, specific prolyl hydroxylases (PHD), Hipple-Lindau tumor suppressor protein (VHL), and factor inhibiting HIF (FIH) were measured by immuno-histochenmistry staining. Osteoclasts derived from OVX-mice were treated with inhibitors of extracellular regulated protein kinases (ERK), protein kinase B (Akt) and nuclear factor kappa B (NF-κB) signaling pathways. HIF-1α expression were detected by Western blot to obtain a rudimentary knowledge of possible mechanism of up-regulation of HIF-1α in osteoclasts of postmenospausal osteoporosis. ResultsMetabolism product of mouse bone tissue of B group were higher than A group ( P P P P
