Abstract
Objective: The overall objective of this study was to investigate the effects of catalpol on bone remodeling of diabetic osteoporosis by regulating osteoblast differentiation and migration. Method: Using a murine model of diabetic osteoporosis, to detect the protective effects of catalpol on bone loss, architectural deterioration of trabecular bone and bone metabolism biomarkers were tested. A model of MC3T3-E1 cells was established by treatment with high glucose; the regulatory role of catalpol in the differentiation and migration was tested by Western blot, ALP staining, and Alizarin Red staining. Results: Catalpol treatment markedly ameliorated trabecular bone deterioration by reducing degenerative changes of the trabecular structure by improving the bone formation marker levels of ALP, osteopontin, type I collagen, and osteocalcin, as well as the level of OPG/RANKL. Catalpol enhanced cell motility and scattering following gap formation of MC3T3-E1 cells. Conclusion: The results indicated that catalpol exhibits a protective effect against diabetic osteoporosis by regulating the differentiation and migration of osteoblast.
Highlights
Accumulating evidence has shown that diabetes is associated with an increased risk of osteoporosis and fragility fractures
The mice were fed with 55% highfat diet fed (4 weeks) and intraperitoneally injected with streptozotocin (0.5% of STZ solution was prepared in 0.1 mol citrate buffer, using 1 ml syringe) at a dose of 40 mg/kg for five consecutive days to build type 2 diabetes osteoporosis model (Xie et al, 2018)
The observed degeneration in trabecular bone structure in the model group compared with the normal group and the degeneration of femurs were clearly inhibited by the treatment with catalpol
Summary
Accumulating evidence has shown that diabetes is associated with an increased risk of osteoporosis and fragility fractures. The presence of low bone mineral density (BMD) and delay in fracture healing in diabetic patients have begun to receive more attention (Kanazawa et al, 2018). Research proves that patients with type 2 diabetes have greater trabecular but lower cortical BMD (Kanazawa et al, 2018). In the progression of diabetes, hyperinsulinemia as well as the relative impairment of glucose metabolism suppresses bone formation, which explains the discrepant results of BMD (Vestergaard, 2007). The adverse impact of hyperglycemia and oxidative stress induced by high glucose on bone formation plays a critical part in the etiology of the bone loss of diabetic osteoporosis (Pereira et al, 2017). High-level blood glucose and advanced glycation end-products (AGEs), activation of protein kinase C isoforms, glucose
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