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Previous research has reported that salidroside exerts antitumor properties on numerous types of tumor cells; however, its effect on osteosarcoma cells remains unknown. The present study aimed to investigate the effects of salidroside on the viability, apoptosis and invasion of osteosarcoma cells in vitro , and determine the underlying mechanism of action. The results of an MTT revealed that salidroside suppressed the viability of osteosarcoma cells (MG63 and U2OS cells) in a time- and concentration-dependent manner. The results of cell morphological analysis (profile observations and Hoechst 33258 staining) and the detection of apoptosis by flow cytometry further indicated that the decrease in osteosarcoma cell viability induced by salidroside was associated with cell apoptosis. Western blot analysis not only confirmed these results but also suggested that salidroside induced the apoptosis of osteosarcoma cells by activating the caspase-9-dependent apoptotic pathway. In addition, we reported that salidroside induced G 0 /G 1 phase arrest and suppressed the invasion of osteosarcoma cells, as measured by flow cytometric cell cycle analysis and a Transwell invasion assay, respectively. Western blot analysis confirmed the aforementioned results. Furthermore, our findings demonstrated that salidroside induced the apoptosis, G 0 /G 1 phase arrest and suppressed the invasion of osteosarcoma cells by inhibiting the janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway, as determined by western blot analysis. In summary, the findings of the present study suggested that salidroside may inhibit the progression of osteosarcoma by suppressing the growth and invasion of osteosarcoma cells. Furthermore, the investigations into the underlying mechanism demonstrated that salidroside exerted notable antitumor activity in osteosarcoma cells by inhibiting the JAK2/STAT3 signaling pathway.

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Oxidative stress is the crucial pathogenic factor in osteoporosis. Cell autophagy, a major form of self-digestion, plays critical functions in different forms of stress by devouring harmful cytosolic proteins or organelles for the renewal of organelles and to maintain cellular homeostasis. Glucosamine (GlcN) has been widely utilized in treatments for patients with osteoarthritis-related joint pain. It has potential antioxidant effects and its pharmacological effect in osteoblasts remains unclear.The present study aimed to investigate whether autophagy participates in the protective effects of GlcN in osteoblasts under oxidative stress and the possible mechanism. First of all, MC3T3-E1 cells were treated with hydrogen peroxide (H 2 O 2 ) to induce oxidative stress, as assessed by viability assays, apoptosis, the intracellular reactive oxygen species production. GlcN was capable of inducing autophagy and protected osteoblasts from those cytotoxic effects. Moreover, it significantly attenuated H 2 O 2 -induced oxidative stress as measured by malondialdehyde, glutathione, nitrite, and superoxide dismutase levels. Importantly, the autophagy level increased in osteoblasts treated with GlcN as represented by an increase in both Beclin1 expression and the LC3 II/I ratio. Immunofluorescence analysis of autophagosomes also confirmed the above results. In addition, GlcN decreased the mammalian target of rapamycin (mTOR) and protein kinase B (Akt). However, the Akt activator (SC79) suppressed the autophagy level induced by GlcN in osteoblasts.Consequently, the antioxidant effects of GlcN were mediated, at least in part, by enhancing autophagy through the Akt/mTOR pathway. These results suggested that GlcN might be a promising candidate for osteoporosis treatment.