Calcium phytate reverses high glucose‐inhibited osteogenesis of BMSCs via the MAPK/JNK pathway

Abstract

AbstractObjectivesDiabetes mellitus (DM) induces oxidative tissue impairment and suppresses bone formation. Some studies have shown that phytic acid has antioxidant and anti‐diabetic properties. This study aimed to investigate the potential of calcium phytate (Ca‐phytate) to reverse inhibited osteogenesis of human bone marrow mesenchymal stem cells (hBMSCs) in a high glucose (HG) environment and to determine the underlying mechanism.Materials and MethodshBMSCs were exposed to HG and palmitic acid to simulate DM in vitro. Osteogenic differentiation was measured using alkaline phosphatase staining and activity assay, alizarin red S staining, qRT‐PCR, Western blot and immunofluorescence staining. A critical‐size cranial defect model of type 2 diabetes mellitus (T2DM) rats was established to evaluate bone regeneration. A specific pathway inhibitor was used to explore whether the MAPK/JNK pathway was involved.ResultsTreatment with 34 μM Ca‐phytate had the highest effect on osteogenic differentiation in HG. Ca‐phytate improved cranial bone defect healing in T2DM rats. The long‐term HG environment inhibited the activation of the MAPK/JNK signalling pathway, which was restored by Ca‐phytate. Blocking the JNK pathway reduced the Ca‐phytate‐mediated osteogenic differentiation of hBMSCs.ConclusionCa‐phytate induced bone regeneration in vivo and reversed HG‐inhibited osteogenesis of hBMSCs in vitro via the MAPK/JNK signalling pathway.