Salidroside promoted osteogenic differentiation of adipose-derived stromal cells through Wnt/β-catenin signaling pathway

BackgroundBone disease causes short-term or long-term physical pain and disability. It is necessary to explore new drug for bone-related disease. This study aimed to explore the role and mechanism of Salidroside in promoting osteogenic differentiation of adipose-derived stromal cells (ADSCs).MethodsADSCs were isolated and treated with different dose of Salidroside. Cell count kit-8 (CCK-8) assay was performed to assess the cell viability of ADSCs. Then, ALP and ARS staining were conducted to assess the early and late osteogenic capacity of ADSCs, respectively.Then, differentially expressed genes were obtained by R software. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the differentially expressed genes were further analyzed. The expression of OCN, COL1A1, RUNX2, WNT3A, and beta -catenin were measured by real-time PCR and Western blot analysis. Last, beta -catenin was silenced by small interfering RNA.ResultsSalidroside significantly increased the ADSCs viability at a dose-response manner. Moreover, Salidroside enhanced osteogenic capacity of ADSCs, which are identified by enhanced ALP activity and calcium deposition. A total of 543 differentially expressed genes were identified between normal and Salidroside-treated ADSCs. Among these differentially expressed genes, 345 genes were upregulated and 198 genes were downregulated. Differentially expressed genes enriched in the Wnt/beta -catenin signaling pathway. Western blot assay indicated that Salidroside enhanced the WNT3A and beta -catenin expression. Silencing beta -catenin partially reversed the promotion effects of Salidroside. PCR and Western blot results further confirmed these results.ConclusionSalidroside promoted osteogenic differentiation of ADSCs through Wnt/beta -catenin signaling pathway.

Automated summary

Salidroside enhanced the osteogenic differentiation of ADSCs through the Wnt/beta-catenin signaling pathway, as confirmed by increased cell viability, ALP activity, and calcium deposition, as well as upregulation of WNT3A and beta-catenin expression.