u-0126 has been researched along with hesperetin* in 1 studies
1 other study(ies) available for u-0126 and hesperetin
| Article | Year |
|---|---|
Hesperetin alleviated glucocorticoid-induced inhibition of osteogenic differentiation of BMSCs through regulating the ERK signaling pathway.
The objective of this study is to investigate the protective role of hesperetin for the glucocorticoid-induced osteoporosis (GIOP) and related mechanisms. In this study, we investigated the protective effects of hesperetin on dexamethasone (DEX)-induced osteogenic inhibition in bone marrow mesenchymal stem cells (BMSCs). The mineralization, real-time quantitative polymerase chain reaction assays (RT-qPCR), immunofluorescence and western blot were used to assess the protective effects of hesperetin in DEX-treated BMSCs during osteogenic differentiation. Our results showed that hesperetin promoted alkaline phosphatase (ALP) activity and the mineralization in DEX-treated BMSCs during osteogenic differentiation. The expression of osteogenic mRNA and proteins further confirmed the protective effect of hesperetin in DEX-treated BMSCs. Furthermore, hesperetin activated ERK signal pathway in DEX-treated BMSCs. ERK inhibitor U0126 could abolish the protective effect of hesperein in DEX-treated BMSCs. In conclusion, our study demonstrated that hesperetin alleviated glucocorticoid-induced inhibition of osteogenic differentiation through ERK signal pathway in BMSCs. It may be a potential therapeutic agent for protecting against glucocorticoid-induced osteoporosis. Topics: Butadienes; Cell Differentiation; Dexamethasone; Extracellular Signal-Regulated MAP Kinases; Glucocorticoids; Hesperidin; Humans; MAP Kinase Signaling System; Mesenchymal Stem Cells; Nitriles; Osteogenesis; Osteoporosis; Primary Cell Culture | 2021 |