ADIPONECTIN INHIBITS OSTEOCLAST DIFFERENTIATION INDUCED BY RANKL AND ITS MECHANISM

Objective: To analyze the mechanism of adiponectin inhibiting the differentiation of osteoclasts induced by RANKL. Methods: Bone marrow mononuclear cells were extracted in vitro. Osteoclasts were induced and cultured by RANKL (100 ng/ ml) and M-CSF (50 ng/ml) and then divided into an adiponectin (10 ng/ml) group and a blank control group. TRAP staining was used to detect the number of osteoclasts, real-time quantitative PCR was used to detect the expression of RANKL, Oscar, TRAP and cathepsin K genes, flow cytometry was used to detect the expression of AdipoR1 on the surface of osteoclast precursor cells and Western blotting was used to detect the protein phosphorylation level of mTOR and 4ebp1. Results: The number of osteoclasts in the adiponectin group was significantly lower than that measured in the control group (P<0.05). The levels of RANKL, Oscar, TRAP and cathepsin K mRNA in osteoclasts of the adiponectin group was significantly lower than that measured in the control group (P<0.05). The expression of AdipoR1 on the surface of osteoclast precursor cells in the adiponectin group was significantly higher than that measured in the control group (P<0.05). The protein levels of p-mTOR and p-4ebp1 in osteoclasts in the adiponectin group were significantly lower than those measured in the control group (P<0.05). Conclusion: Adiponectin can inhibit the differentiation and maturation of osteoclasts induced by RANKL. The mechanism may be related to the increase of the expression of AdipoR1 on the surface of osteoclast precursor cells and the inhibition of p-mTOR and p-4ebp1.