Omentin‑1 induces osteoblast viability and differentiation via the TGF‑β/Smad signaling pathway in osteoporosis

Osteoporosis is a bone‑related disease that results from impaired bone formation and excessive bone resorption. The potential value of adipokines has been investigated previously, due to their influence on osteogenesis. However, the osteogenic effects induced by omentin‑1 remain unclear. The aim of the present study was to determine the regulatory effects of omentin‑1 on osteoblast viability and differentiation, as well as to explore the underlying molecular mechanism. The present study investigated the effects of omentin‑1 on the viability and differentiation of mouse pre‑osteoblast cells (MC3T3‑E1) using quantitative and qualitative measures. A Cell Counting Kit‑8 assay was used to assess the viability of MC3T3‑E1 cells following treatment with different doses of omentin‑1. Omentin‑1 and bone morphogenetic protein (BMP) inhibitor were added to osteogenic induction mediums in different ways to assess their effect. The alkaline phosphatase (ALP) activity and Alizarin Red S (ARS) staining of MC3T3‑E1 cells treated with omentin‑1 and/or BMP inhibitor were used to examine the effects of omentin‑1 on differentiation and mineralization. Western blotting was used to further explore its potential mechanism, and to study the role of omentin‑1 on the viability and differentiation of osteoblasts. The results showed that omentin‑1 altered the viability of MC3T3‑E1 cells in a dose‑dependent manner. Omentin‑1 treatment significantly increased the expression of members of the TGF‑β/Smad signaling pathway. In the omentin‑1 group, the ALP activity of the MC3T3‑E1 cells was increased, and the ARS staining area was also increased. The mRNA and protein expression levels of BMP2, Runt‑related transcription factor 2, collagen1, osteopontin, osteocalcin and osterix in the omentin‑1 group were also significantly upregulated. All these effects were reversed following treatment with SIS3 HCl. These results demonstrated that omentin‑1 can significantly promote osteoblast viability and differentiation via the TGF‑β/Smad signaling pathway, thereby promoting bone formation and preventing osteoporosis.