Fig. 7
Pharmacological activation of FXR promoted osteoblast differentiation and partially prevented bone mass loss induced by OVX. a Schematic representation of experimental design of OCA treatment in OVX mice. b–h Representative micro-CT images of distal femurs in Sham, OVX, OVX treated with OCA groups mice with morphometric analysis of bone volume per tissue volume (BV/TV), bone mass density (BMD), trabecular thickness (Tb.Th), trabecular number (Tb.N), trabecular spacing (Tb.Sp) and cortical thickness (Ct.Th) (n = 6). i–k Representative images of calcein double labeling and quantitative analysis of mineralization apposition rate (MAR) and bone formation rate (BFR) from Sham, OVX, OVX treated with OCA groups mice (n = 4). Scale bar = 20 μm. CB means cortical bone. TB means trabecular bone. l, o Representative images of hematoxylin and eosin (HE) staining (l) in the femurs area from Sham, OVX, OVX treated with OCA groups. Adipocyte area (o) was analyzed in accordance with HE staining (n = 5). Scale bar = 500 μm. m, p Immunohistochemistry staining (m) and quantification (p) of Sp7 (Osx, an osteoblastic lineage cell marker) in the femurs of mice (n = 5). Scale bar = 50 μm. q Elisa analysis of serum PINP (ng/ml) from Sham, OVX, OVX treated with OCA groups mice (n = 6). n TRAP staining of femur area from sham, OVX, OVX treated with OCA groups (n = 6). Scale bar = 50 μm. *P < 0.05, **P < 0.01. Data are represented as mean ± SEM
