Icariin (ICA), a Traditional Chinese Medicine, has been demonstrated to be a promoting compound for extracellular matrix synthesis and gene expression of chondrocytes. However, whether ICA can act as a substitute for or cooperate with growth factors to directly promote stable chondrogenesis of bone marrow mesenchymal stem cells (BMSCs) remains unknown. In the present study, rat BMSCs were cultivated in monolayer cultures with a chondrogenic medium containing transforming growth factor‑β3 for 14 days; ICA was added to the same chondrogenic medium throughout the culture period at a concentration of 1x10‑6 M. Cell morphology was observed using an inverted microscope, and chondrogenic differentiation markers, including collagen II, aggrecan and SRY (sex determining region Y)‑box 9 (SOX9), were detected by immunofluorescence, reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Hypertrophic differentiation was also analyzed using collagen I gene expression and alkaline phosphatase (ALP) activity. The results revealed that ICA was effective at forming an increased number of and larger aggregates, and significantly upregulated the mRNA expression levels and protein synthesis of collagen II, aggrecan and SOX9. Furthermore, the chondrogenic medium alone caused hypertrophic differentiation through the upregulation of collagen I gene expression and ALP activity, which was not potentiated by the presence of ICA. Thus, ICA promoted directed chondrogenic differentiation of BMSCs, but had no effect on hypertrophic differentiation. The present results also suggested that ICA may be an effective accelerant of growth factors for cartilage tissue engineering by promoting their chondrogenic differentiating effects but reducing the effect of hypertrophic differentiation.

Osteoarthritis (OA) is a disabling disease of joint with no clear treatment. The finding of medicine be of benefit to joint is an important topic for osteoarthritis prevention and treatment. The present study was designed to explore the therapeutic effects and possible underlying mechanism of dioscin, a natural steroidal saponin, on osteoarthritis. OA models were created via intra-joint injection of monosodium iodoacetate (MIA) in rats. After the administration of dioscin, the effects of dioscin were estimated with western blotting, qRT-PCR and histologic staining. The results showed that dioscin exerted cartilage and extracelluar matrix (ECM) protective effects via suppressing ER-stress, oxidative stress, apoptosis and inflammation. More significantly, it also ameliorated the progress of OA via inhibiting Wnt/β-catenin pathway and up-regulating PPAR-γ expression. Our work showed the good protective effects of dioscin on MIA-induced OA for the first time. Dioscin is a promising drug on OA treatment although further researches are needed in the future.

Dioscin, a typical steroid saponin, is isolated from Dioscorea nipponica Makino and Dioscorea zingiberensis Wright. It has estrogenic activity and many studies have also reported that dioscorea plants have an effect in preventing and treating osteoporosis. However, the molecular mechanisms underlying their effect on osteoporosis treatment are poorly understood. Therefore, the present study aims to investigate the mechanism (s) by which dioscin promotes osteoblastic proliferation and differentiation in mouse pre-osteoblast like MC3T3-E1 cells and human osteoblast-like MG-63 cells.

Recently, accumulating evidence has indicated that glucocorticoid-induced osteoporosis (GIOP) is closely related to oxidative stress and apoptosis. Alpha-lipoic acid (LA), a naturally endogenous anti-oxidant, possesses anti-oxidative and anti-apoptosis activities, implicating LA as a therapeutic agent for the treatment of GIOP. In this study, the osteogenesis-promoting effects of LA against GIOP were investigated and the mechanisms were further probed. Here, the results showed that LA inhibited oxidative stress, suppressed apoptosis and improved osteopenia by promoting the expression of osteogenesis markers, including ALP, COL-I, OCN, BMP-2, RUNX2 and OSX. Further study revealed that the osteogenesis-promoting effects of LA likely occur via the regulation of the NOX4, NF-kappaB, JNK and PI3K/AKT pathways. The present study indicated that LA may prevent GIOP and promote osteogenesis and might be a candidate for the treatment of GIOP.