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

被引:13
作者
Liu, Ling [1 ,2 ]
Zheng, Jie [1 ,2 ]
Yang, YaZhen [1 ,2 ]
Ni, Lingjuan [1 ,2 ]
Chen, Hongyu [1 ,2 ]
Yu, Dongrong [1 ,2 ]
机构
[1] Hangzhou Hosp Tradit Chinese Med, Dept Nephrol, Tiyuchang Rd 453, Hangzhou 310007, Zhejiang, Peoples R China
[2] Hangzhou Hosp Tradit Chinese Med, Dept Nephrol, Management Kidney Dis, Key Lab Zhejiang Prov, Tiyuchang Rd 453, Hangzhou 310007, Peoples R China
关键词
Glucocorticoid-induced osteoporosis; Hesperetin; Bone marrow mesenchymal stem cells; ERK; MESENCHYMAL STEM-CELLS; INDUCED OSTEOPOROSIS; PREVENTION; MANAGEMENT;
D O I
10.1007/s00795-020-00251-9
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:1 / 7
页数:7
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