The effect of the α7nAChR agonist on Wnt/β-catenin signaling in osteoporosis.

The cholinergic pathway neurotransmitter acetylcholine (ACh) regulates the inflammatory cascade through a specific α7 nicotinic acetylcholine receptor (α7nAChR). However, the role and related mechanisms of α7nAChR in osteoporosis (OP) remain unclear. Therefore, this study aims to analyze the effects of α7nAChR on osteoblasts and related mechanisms. Mouse osteoblast MC3T3-E1 was cultured in vitro and divided into a control group and an α7nAChR agonist group (2.4 and 4.8 mg/kg.d). An MTT assay was used to detect the osteoblast activity, an ARS staining assay was used to analyze the formation of calcified nodules of osteoblasts, and an alkaline phosphatase (ALP) activity colorimetric assay was used to determine the ALP activity. Real-time PCR was performed to analyze the expression of RUNX2 and OPN mRNA. The inflammatory factor tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) secretions were analyzed by ELISA. The α7nAChR agonists dose-dependently promoted osteoblast proliferation, increased calcified nodules, ALP activity, RUNX2 and OPN mRNA expression, decreased inflammatory factors TNF-α and IL-6 secretion, and increased Wnt1, β-catenin mRNA and protein expression. Compared with the control group, the differences were statistically significant (P<0.05). α7nAChR agonists can inhibit the proliferation and differentiation of osteoblasts by regulating the Wnt/β-catenin signaling pathway, and then participate in the regulation of osteoporosis. IJCEP