唑来膦酸
SOD2
运行x2
化学
间充质干细胞
氧化应激
SIRT3
癌症研究
药理学
碱性磷酸酶
内科学
医学
生物化学
细胞生物学
超氧化物歧化酶
生物
乙酰化
锡尔图因
酶
基因
作者
Jin Zh,SF Wang,Wei Liao
标识
DOI:10.26355/eurrev_202002_20389
摘要
Objective The aim of this study was to clarify the potential effect of zoledronic acid on alleviating oxidative stress and promoting bone marrow mesenchymal stem cells (BMSCs) osteogenesis through the SIRT3/SOD2 pathway, thus alleviating the progression of osteoporosis. Materials and methods Relative expression levels of osteogenesis-related genes (ALP, RUNX2, and Bglap) were determined. Meanwhile, ALP activity and capacity of mineralization in BMSCs treated with different doses of zoledronic acid were measured. Subsequently, viability and ROS level in H2O2-induced BMSCs influenced by zoledronic acid treatment were assessed. The regulatory effect of zoledronic acid on the SIRT3/SOD2 pathway was detected by Western blot. Furthermore, the involvement of the SIRT3/SOD2 pathway in zoledronic acid-mediated BMSCs osteogenesis was evaluated. Results Zoledronic acid treatment significantly up-regulated the levels of ALP, RUNX2, and Bglap. Meanwhile, it improved ALP activity and capacity of mineralization in BMSCs dose-dependently. H2O2 induction markedly suppressed viability and enhanced ROS level in BMSCs, which were reversed by zoledronic acid treatment. Besides, zoledronic acid protected H2O2-induced SIRT3 down-regulation and AC-SOD2/SOD2 up-regulation in BMSCs. In addition, silence of SIRT3 reversed the protective effects of zoledronic acid on osteogenesis of BMSCs. Conclusions Zoledronic acid alleviates the progression of osteoporosis. Meanwhile, it accelerates BMSCs osteogenesis by inhibiting oxidative stress via the SIRT3/SOD2 pathway.
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