Figure 9.

Mechanism of anti-osteoporosis effect through modulation of gene expression at the transcriptional and translational level in different kinds of bone cells by daidzein (DZ), genistein (GS), glycetin (GC), and their metabolites (6-hydroxydaidzein (6-HD), formononetin (FNT), dihydrodaidzein (DHD), biochain A (BCA), and cladrin). Cell differentiation and proliferation, osteogenic activity, and bone health (such as bone density) are enhanced, whereas cell apoptosis, bone loss, and bone resorption are attenuated in cells (MG-63, MC3T3-E1, Saos-2, and bone marrow) and rats/mice [9]. ALP, alkaline phosphatase; B.Ar, bone area; BMP2, bone morphogenetic protein 2; BV/TV, bone volume/tissue volume; Ca²⁺, calcium ion; C/EBP-α, CCAAT/enhancer-binding protein alpha; Col1a, collagen type 1; c-Fos, cellular oncogene fos; CTSK, cathepsin K; ERAα/β, estrogen receptor A alpha/beta; NFATc1, nuclear factor of activated T-cells cytoplasmic 1; OCN, osteocalcin; OPG, osteoprotegerin; PPARγ, peroxisome proliferator-activated receptor-gamma; RANKL, receptor of activator of nuclear factor kappa B ligand; RUNX2, runt-related transcription factor 2; SMI, structure model index; T3, triiodothyronine; T4, thyroxine; Tb.N, trabecular number; Tb.Pf, trabecular pattern factor; Tb.Sp, trabecular separation; Tb.Th, trabecular thickness; TNF-α, tumor necrosis factor-α; TRAP, tartrate-resistant acid phosphatase; Wnt/β-catenin, canonical Wnt pathway; ↑, enhancing; ↓, lowering; →, activation; ˧, inhibition. Figure adapted from Hsiaoa, Y.H. et al. [9].