Conclusions
CES promotes fracture healing by promoting osteoblastogenesis via a partial BMP2-Smad pathway.
Methods
Fifty-four C57BL/6 male mice underwent femoral shaft fracture by Bonnarens and Einhorn's method, subsequently receiving a water extract of CES (200 mg/kg/day, daily) for 7 and 14 days. Safranin O staining and immunohistochemistry of the fracture region were conducted against transforming growth factor-β (TGF-β), bone morphogenetic protein 2 (BMP2), and osterix. MG63 cells used to examine the underlying mechanisms of CES focused on BMP2-Smad pathway-related osteogenesis.
Results
CES administration led to earlier union of the fractured bones, supported by Safranin O staining of the fracture region, demonstrating significantly increased cartilage formation day on 7 and a rapidly decreased cartilage area due to callus formation day on 14. CES administration also significantly upregulated the expression of TGF-β1 day 7, BMP 2, and osterix day 14 at the fracture site and also up-regulated alkaline phosphatase (ALP) activity, calcium deposition, and the phosphorylation of Smad in MG63 cells. Conclusions: CES promotes fracture healing by promoting osteoblastogenesis via a partial BMP2-Smad pathway.