Effects of rhPTH(1-34)treatment for glucocorticoid-induced osteoporosis / 实用医学杂志

ABSTRACT

Objective To establish the GIOP model and extract BMSCs from the rat model.We aim to in-vesitigatethe effect ofrhPTH(1-34)for inhibiting β-catenin ubiquitination when combining with Micro-CT and bio-logical technology.We also investigate the influence of rhPTH(1-34)on the GIOP.Methods Female SPF emale rats wererandomly divided into normal control group,methylprednisolone group(model group),methylpredniso-lone+saline group(blankcontrol group)and methylprednisolone+rhPTH(1-34)group(test group). The proximal femoral cancellous bone was examined by Micro-CTand histopathological Staining. The expression of Wnt10b and β-catenin protein were detected. By comparing with inducedBMP-2,BMSCs were treated withrhPTH(1-34)and stained with ALP and alizarin red.Results(1)In Micro-CT,BV/TV,Tb.Th and Tb/N decreased,whereas Tb/sp increased in the test group comparedwith model group(P<0.05).ROI three-dimensional reconstruction of trabecu-lar bone in test group showed local bone repair;(2)Wnt10b and β-cateninexpression increased in the test group compared with the model model(P<0.05),indicating that rhPTH(1-34)can enhance the transcriptional activity of β-catenin(P<0.05)and promote the expression of Wnt10b andβ-catenin(P<0.05).Conclusion The inter-vention with rhPTH(1-34)can prevent GIOP by regulating the Wnt/β-catenin signaling pathway and inhibiting GIOP progress,which can improve the microstructure of bone.