Oxidative stress are the crucial pathogenic factors 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 remain unclear. The present study aimed to investigate whether autophagy participates 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 (H2O2) to induce oxidative stress, as assessed by viability assays, apoptosis, the intracellular ROS production. GlcN was capable of inducing autophagy and protected osteoblasts from those cytotoxic effects. Moreover, it significantly attenuated H2O2-induced oxidative stress as measured by malondialdehyde (MDA), glutathione (GSH), nitrite and superoxide dismutase (SOD) level. Importantly, the autophagy level increased in osteoblasts treated with GlcN as represented by an increased 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.

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