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Type 2 diabetic osteoporosis (T2DOP) has become a common secondary cause of osteoporosis that accelerates bone loss and leads to bone fractures. The aim of the current study was to investigate the association between the anti-osteoporotic effect of curcumin (Cur) and the transforming growth factor (TGF)β/Smads signaling pathway. Male Sprague-Dawley rats were used in the experiments. The type 2 diabetes mellitus (T2DM) animals were treated with Cur for 8 weeks and blood lipid markers, bone microstructure and bone biomechanics were then evaluated. The mRNA expression levels of TGFβ1, type I TGFβ receptor (TβRI), TβRII and Smad2/3 were determined using reverse transcription-quantitative PCR (RT-qPCR) and immunohistochemistry. The body weight of rats with type 2 diabetes-induced osteoporosis increased (P&lt;0.05), while the lipid (total cholesterol, triglyceride and low-density lipoprotein) and fasting blood glucose levels were decreased by Cur (P&lt;0.05). In addition, Cur significantly improved bone biomechanical properties (maximum load, breaking load, elastic load and the bone rigidity coefficient) and preserved bone microarchitecture (P&lt;0.05). The RT-qPCR and IHC results revealed that Cur increased TGFβ1, TβRI, TβRII and Smad2/3 expression levels and promoted Smad2/3 phosphorylation in bones. The present results also indicated that Cur regulated lipid and glucose levels, improved bone biomechanical properties and preserved bone microarchitecture, and that these effects may be mediated via TGFβ/Smad2/3 pathway activation.

Curcumin protects bone biomechanical properties and microarchitecture in type�2 diabetic rats with osteoporosis via the TGFβ/Smad2/3 pathway