Aluminum (Al) can accumulate in bone and cause bone diseases. Few studies have investigated molecular mechanism of Al-induced bone diseases. Thus, in this study, rats were orally exposed to 0 (control group) and 0.4 g/L aluminum trichloride (AlCl3) (treatment group) for 30, 60, 90 or 120 days, respectively. The Al content of femora and serum, bone histological structure, bone mineral density (BMD) of the distal and proximal femoral metaphysis and Wnt/β-catenin signaling pathway (the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5) in rat femora were determined on day 30, 60, 90 or 120, respectively. The results showed that the Al contents of femora and serum were increased, the BMD of the distal and proximal femoral metaphysis were decreased, the femora histological structure were disrupted, the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5 were all decreased in the treatment group compared with the control group with time prolonged. These results indicated that AlCl3 impaired femora by inhibiting the Wnt/β-catenin signaling pathway in young growing rats.
Keywords: Aluminum trichloride; Femora; Rat; Wnt/β-catenin signaling pathway.
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