It is known that canonical Wnt/b-catenin is a key pathway for regulating bone

Formation and remodeling and contributes to osteoblastic differentiation, of which DKK-1 is one of the inhibitor in Wnt-signaling. Studies demonstrate GC to be Erlotinib|CP-358774|OSI-774|NSC-718781 EGFR/HER2 inhibitor a very strong inducer of DKK-1 protein which leads to a decrease in osteoblast bone formation in GC induced osteoporosis. Moreover, Runx2 was found to integrate Wnt-signaling for mediating osteogenic differentiation of MSCs, it was known to be involved in BMP signaling as mentioned earlier. Our in vivo observation further demonstrated that Sal B stimulated femur bone BMP-2 and BMP-7 mRNA expression and protected GC-treated rats from decrease of femur bone BMP-2 and BMP-7 protein expression. BMP/Wnt/b-catenin share a crossover mechanism for stimulation of progenitor, osteoblast and angiogenetic generation,Everolimus|RAD001}|{Everolimus|RAD001}|{Everolimus|RAD001} mTOR inhibitor thus our study support the idea that Sal B protected against GC-induced osteoblast impairment associated abnormal angiogenesis and adipogenesis. Recently Lu et al. reported that Sal B protected against oxidative stress– induced apoptosis in rat bone marrow stem cells suggesting that Sal B may inhibit GC-induced bone marrow stem cell apoptosis to enlarge the local pool of osteoblast precursors available for osteogenesis.