Abstract

Oxidative stress causes damage and apoptosis of bone marrow mesenchymal stem cells (BMSCs). Osteoprotegerin (OPG) regulates bone differentiation. However, whether OPG plays a role in osteogenic/adipogenic differentiation under oxidative stress remains poorly understood. Rat BMSCs were randomly divided into control group; H2O2 group, in which H2O2 was used to prepare oxidative stress model; OPG group, in which 5 μM OPG was added to BMSCs based on oxidative stress model followed by analysis of BMSCs proliferation by MTT assay, BMSCs apoptosis, expression of RUNX2, OPN, FABP4 and PPARγ2 by real time PCR, OPG and RANKL protein expression by Western blot as well as SOD activity and ROS content by spectrophotometry. Compared with control group, H2O2 significantly decreased BMSCs proliferation, increased Caspase 3 activity, downregulated RUNX2 and OPN, upregulated FABP4 and PPARγ2, decreased SOD activity and increased ROS content (P < 0.05). Under H2O2 treatment, OPG addition significantly promoted BMSCs proliferation, decreased Caspase 3 activity, increased RUNX2 and OPN expression, decreased FABP4 and PPARγ2 expression, increased SOD activity, and decreased ROS content and RANKL expression (P < 0.05). OPG can promote osteogenic differentiation of BMSCs under oxidative stress, inhibit adipogenic differentiation, and protect BMSCs from damage and promote BMSCs proliferation by regulating OPG/RANKL signaling pathway.

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