title: Genistein attenuates glucocorticoid-induced bone deleterious effects through regulation Eph/ephrin expression in aged mice.
abstract: This study was performed to investigate bone deteriorations and the involvement of skeletal Eph/ephrin signaling pathway of GIOP aged mice in response to the treatment of genistein.
  
  
  
  The biomarkers in serum and urine were measured, tibias were taken for the measurement on gene and protein expression and histomorphology analysis, and femurs were taken for the measurement on bone Ca and three-dimensional architecture of trabecular bone.
  
  
  
  Genistein showed a greater increase in bone Ca, BMD and significantly increased FGF-23 and OCN, reduced TRACP-5b, PTH and CTX in GIOP mice. Genistein reversed DXM-induced trabecular deleterious effects and stimulated bone remodeling. The treatment of DXM group with genistein significantly elevated the ratio of OPG/RANKL. Moreover, genistein administration down-regulated the mRNA and protein expression of Eph A2 and ephrin A2 in tibia of the GIOP mice. In contrast, the mRNA and protein expression of Eph B4 and ephrin B2 were increased in mice treated by DXM with genistein as compared to the DXM single treatment.
  
  
  
  DXM-induced trabecular bone micro-structure deterioration in aged mice was involved in the regulation of the Eph receptors and ephrin ligands. Genistein might represent a therapy with bone-forming as well as an anti-resorptive activity in GIOP mice. The underlying mechanism was mediated, at least partially, through regulation Eph/ephrin signaling.
authors.affiliation: Department of Endocrinology, The Second Affiliated Hospital of Anhui Medical University 678 Furong Road, Hefei 230601, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Cheng
authors.affiliation: 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, The Key Laboratory of Hormones and Development (Ministry of Health), Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University 66 Tongan Road, Tianjin 300070, China.
authors.forename: Wei-Lin
authors.initials: WL
authors.lastname: Wang
authors.affiliation: Department of Neurosurgery, The People's Hospital of Anqiu 246 Jiankang Road, Weifang 262100, China.
authors.forename: Jun-Jun
authors.initials: JJ
authors.lastname: Liang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D015519:Bone Density / Q000187:drug effects; D001842:Bone and Bones / Q000187:drug effects* / Q000378:metabolism; D003907:Dexamethasone / Q000009:adverse effects; D036342:Ephrins / Q000096:biosynthesis*; D005260:Female; D000089703:Fibroblast Growth Factor-23; D019833:Genistein / Q000494:pharmacology*; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D036081:Receptors, Eph Family / Q000096:biosynthesis*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D036342:Ephrins; C000717427:FGF23 protein, human; C000717428:Fgf23 protein, mouse; D005938:Glucocorticoids; D047428:Protein Kinase Inhibitors; D000089703:Fibroblast Growth Factor-23; D003907:Dexamethasone; D019833:Genistein; D036081:Receptors, Eph Family
keywords: Eph/ephrin; bone; dexamethasone; genistein