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Hesperetin alleviated glucocorticoid-induced inhibition of osteogenic differentiation of BMSCs through regulating the ERK signaling pathway

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Abstract

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.

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Acknowledgements

This work was supported by the Zhejiang Provincial Natural Science Foundation of China (No. LQ18H050005) and Hangzhou Science and Technology Bureau Fund (No.20160533B61), Public welfare projects of Zhejiang Science and Technology Department (No.2018KY613), Zhejiang Traditional Chinese Medicine Bureau Fund (No.2019ZA086).

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Correspondence to Hongyu Chen or Dongrong Yu.

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Liu, L., Zheng, J., Yang, Y. et al. Hesperetin alleviated glucocorticoid-induced inhibition of osteogenic differentiation of BMSCs through regulating the ERK signaling pathway. Med Mol Morphol 54, 1–7 (2021). https://doi.org/10.1007/s00795-020-00251-9

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