Dioscin Promotes Proliferation of Pancreatic Beta Cells via Wnt/β-Catenin Signaling Pathways

Background: Dysfunction of pancreatic beta cells is related with type 2 diabetes mellitus. Dioscin, a natural steroid saponin, has many pharmacological effects. The aim of this study was to investigate the effects of dioscin on apoptosis of pancreatic beta cells induced by high glucose. Methods: Pancreatic cell line RNAKT-15 was treated with 20 mM glucose with or without different concentrations of dioscin and viability and apoptosis of cells were measured. Western blot assay was used to measure the expression levels of some proteins such as phosphorylated glycogen synthase kinase 3 beta (GSK-3 beta) and beta-catenin. Enzymelinked immunosorbent assay (ELISA) was used to detect the pro-inflammatory cytokines. Results: High-glucose could significantly increase cell RNAKT-15 apoptosis and reduce cell viability (p < 0.01). Dioscin could improve the cell degeneration (p < 0.05). The results demonstrated that high-glucose could increase the proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), interferon-gamma (INF-gamma), and transforming growth factor-beta (TGF-beta), while these effects were reduced when treated with dioscin (p < 0.05). Western blot results demonstrated that high-glucose affects p-GSK 3 beta and beta-catenin expression levels (p < 0.01) and dioscin could significantly reduce these two protein levels (p < 0.05). Conclusions: The effects of dioscin against high-glucose induced apoptosis of pancreatic cells may occur through the Wnt signaling pathway. High-glucose led to increased pancreatic cell apoptosis and dioscin could attenuate these impairments. These findings highlight an important role of dioscin in the treatment potential of type 2 diabetes mellitus (T2DM).