BMPs play a major role in the growth and differentiation of osteoblastic cells and have been shown to be potent stimulators of bone formation in various animal models. BMP-2 stimulates the expression of osteogenic genes, Imatinib concentration such as OCN and ALP [26]. Furthermore, osteogenic BMPs such as BMP-2 and BMP-7 have recently been approved for clinical application in spinal fusion, fracture healing, and dental tissue engineering. Anabolic agents that stimulate BMP expression or its signaling pathway can be used to treat osteoblast-related diseases via

bone formation or regeneration [27] and [28]. Loss of both BMP-2 and -4 has been shown to result in severe impairment of osteogenesis [29]. The network of activities and molecular switches for bone development and osteoblastic differentiation involves BMP-induced transcription factors such as RUNX2. RUNX2 is one of

the osteogenic master transcription factors, and its activity is increased by BMP-2 signaling [30] and [31]. In this study, we observed that the mRNA levels of ALP, OCN, OPN, RUNX2, and BMPs (BMP-2, -6, -7, and -9) in cells treated with both Dex and KRG were slightly higher than those in cells treated with only Dex. Current research efforts aim to prevent GC-induced osteoporosis and decrease the incidence of fractures. However, few studies have investigated how to improve the repair of MAPK Inhibitor Library price fractures that have occurred during GC treatment. A parathyroid hormone-related protein analog has been shown to be effective for impaired bone healing in rabbits receiving corticosteroid therapy. Receptor activator of nuclear factor kappa-B ligand (RANKL), BMP-2, and BMP-7 have been shown to inhibit bone loss in GC-treated animals [32]. In addition, the current study verified that KRG increased bone formation in GC-induced osteoporosis mice model. In conclusion, GCs have significant pharmacological effects on bone metabolism, including suppression of bone formation and bone resorption. We observed that KRG prevented synthetic GC (Dex)-induced apoptosis of MC3T3-E1 cells by inhibiting the activation

of caspase-3 and -9. Gene expression of the osteogenic gene markers (ALP, OCN, OPN, Runx2, and BMPs) Clomifene was enhanced in cells treated with both Dex and KRG compared to that in cells treated with Dex only. Furthermore, our data indicate that KRG-treated cells not only activated p-AKT, but also inhibited p-JNK. KRG also increased bone formation in GC-induced osteoporosis mice. Thus, KRG can be used as a beneficial therapeutic for the prevention or treatment of GC-induced osteoporosis. none. This research was sponsored by the grant 2012 from the Korea Ginseng Corporation (GS302-38). The animal experiment in this study was supported by the Experimental Animal Ethics Committee at Gachon University (GC2012-0118).