Fufang Zhenzhu Tiaozhi Capsules regulates MEKK2-Wnt coupling and antagonizes β-catenin ubiquitination to improve glucocorticoid osteoporosis in rats

  Objective: To study the regulatory effects of mitogen-activated protein kinase kinase kinase 2 (MEKK2)-Wnt coupling and Pearlia Odycapsule (FTZ) intervention. FTZ is a compound that antagonizes β-catenin ubiquitination and changes in bone mass. Cells that affect bone formation.

  Method: Male SPF rats were randomly divided into normal control group, methylprednisolone group (model group), methylprednisolone + saline group (blank control group), methylprednisolone + FTZ group (experimental group). Micro-CT examination and histopathological staining were performed on the cancellous bone of the proximal femur to measure the expression of Wnt3a, MEKK2 and β-catenin. Model BMSCs were extracted and stained after FTZ-containing serum, alkaline phosphatase intervention, bone formation and differentiation-related genes ALP, Runx2, OCN expression determination, MEKK2, β-catenin protein expression determination, and β-catenin/TCF transcription level determination. it is.

  Results: 1) Micro CT compares the experimental group and the model group. The former are BV/TV and Tb. Th, Tb/N, etc. decreased, and Tb/sp increased (Pu003c0.05). OI three-dimensional reconstruction showed that the quality of cancellous bone in the experimental group was improved and partially repaired; 2) hematoxylin-eosin staining, the bone trabecular density of the experimental group was higher than that of the model group. ...The cancellous bone is in good condition; 3) The expression of Wnt3a, MEKK2, and β-catenin in the bone tissue of the experimental group was increased compared with that of the model group (Pu003c0.05); 4) BMSC was GIOP. After it was extracted from the rat model and induced BMP2 and FTZ serum intervention (experimental group), the results of alkaline phosphatase and alizarin red staining showed that the bone response of the experimental composition was enhanced (Pu003c0.05); 5) BMSC was β-catenin/TCF transcription. FTZ can increase the activity (Pu003c0.05), interfere and promote the expression of β-catenin and MEKK2 protein (Pu003c0.05).

  Conclusion: FTZ can prevent and treat GIOP by regulating MEKK2-Wnt coupling and antagonizing β-catenin ubiquitination, thereby improving bone structure.