Salidroside promotes osteoblast proliferation and differentiation via the activation of AMPK to inhibit bone resorption of knee osteoarthritis mice

Abstract

AimBalance between osteoclasts and osteoblasts was important for bone development and regeneration, which attracted wide attention. To investigate whether the pro-restorative effect of salidroside (SAL) on knee osteoarthritis in mice was associated with adenosine monophosphate-activated protein kinase (AMPK). MethodsMC3T3-E1 cells were used to perform CCK8, ALP measurement, alizarin red assay and western blot. Mouse model with knee osteoarthritis was constructed and received the treatment of SAL. Body weight, arthritis index, and inflammatory factors were recorded and measured. The paraffin sections of knee bone joints were performed by HE and immunohistochemical staining. Western blot was carried out. CCK8, EDU and flow cytometry were used to analyzed the inhibitory effect of salidroside on osteoclast. ResultsWe found that salidroside could promote osteoblast proliferation and differentiation, and upregulate COL1A1, RUNX2 and OCN proteins and increase ALP content and phosphorylation level of AMPK. In vivo assays showed that salidroside inhibited inflammatory reaction, improved pathological condition. Salidroside reduced TRAP and NFATc1 expression, and increased the expression of ALP, COL1A1, RUNX2 and OCN proteins. p-AMPK protein was upregulated by salidroside treatment. We also performed in vitro assay, and found salidroside could inhibit proliferation of osteoclast and increase apoptosis of osteoclast. ConclusionIn a word, salidroside promoted osteoblast proliferation and differentiation through AMPK activation to further inhibit osteoclast bone resorption, so as to achieve the purpose of relieving knee osteoarthritis.