21:T463,Chondrogenesis and subsequent osteogenesis of mesenchymal stem cells (MSCs) and angiogenesis at injured sites are crucial for bone fracture healing. Amygdalin, a cyanogenic glycoside compound derived from bitter apricot kernel, has been reported to inhibit IL-1β-induced chondrocyte degeneration and to stimulate blood circulation, suggesting a promising role of amygdalin in fracture healing. In this study, tibial fractures in C57BL/6 mice were treated with amygdalin. Fracture calluses were then harvested and subjected to radiographic, histological, and biomechanical testing, as well as angiography and gene expression analyses to evaluate fracture healing. The results showed that amygdalin treatment promoted bone fracture healing. Further experiments using MSC-specific transforming growth factor- (TGF-) β receptor 2 conditional knockout (KO) mice (Tgfbr2^Gli1-Cre ) and C3H10 T1/2 murine mesenchymal progenitor cells showed that this effect was mediated through TGF-β/Smad signaling. We conclude that amygdalin could be used as an alternative treatment for bone fractures.22:T434,Although osteoarthritis (OA) in the hip joint is a common and debilitating degenerative disease, the precise molecular mechanisms underlying its pathological process remains unclear. This study sets out to investigate whether β-catenin plays a critical role in hip OA pathogenesis. Here, we showed overexpressed β-catenin protein in human OA cartilage tissues. Then, we analyzed β-cat(ex3)^Col2ER mice, in which β-catenin gene was conditionally activated in femoral head chondrocytes. At 2 months of age, β-cat(ex3)^Col2ER mice already showed a phenotype of severe cartilage degeneration in the femoral head. More changes observed in β-cat(ex3)^Col2ER mice with age included subchondral sclerosis and osteophyte formation along joint margins, resembling a hip OA phenotype in humans. In addition, cartilage degradation and chondrocyte apoptosis as the results of β-catenin activation possibly contributed to this hip OA-like phenotype. Overall our findings provide direct evidence about the importance of β-catenin in hip OA pathogenesis.23:T572,

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