地塞米松诱导成骨细胞凋亡的作用具有持续时间和剂量依赖性。

Pub Date : 2021-08-28
Xintong Guo, Xiangying Ding, Qinpei Ding, Min Liang
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引用次数: 0

摘要

目的:成骨细胞在成骨和预防骨坏死的过程中发挥着重要作用。地塞米松是糖皮质激素(GCs)的一种,可诱导成骨细胞凋亡,导致非创伤性骨坏死的发生。本研究旨在探讨不同剂量和持续时间的地塞米松对大鼠体外成骨细胞凋亡的影响:方法:采用细胞计数试剂盒-8(CCK-8)检测和 FITC-Annexin V/PI 染色检测地塞米松处理后成骨细胞的增殖和凋亡。使用 Western 印迹和 qRT-PCR 分析了地塞米松处理后成骨细胞中 caspase-3 和 -9 的表达。结果表明,地塞米松能显著抑制成骨细胞的增殖并诱导其凋亡,其作用呈剂量和时间依赖性:结果:随着干预时间的延长,不同地塞米松组caspase-3 mRNA和caspase-9 mRNA的表达量逐渐增加,且呈时间依赖性。在相同的干预时间(12h、24h、48h)内,caspase-3和-9 mRNA的表达呈剂量依赖性逐渐增加。5*10-8M、5*10-7M、5*10-6M和5*10-5M地塞米松处理24小时后,裂解的caspase-3和-9蛋白的表达呈剂量依赖性增加:结论:地塞米松可诱导成骨细胞凋亡,且具有时间和剂量依赖性。
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Dexamethasone induce osteoblast apoptosis in a duration- and dose-dependent manner.

Objectives: Osteoblasts play an important role in the process of osteogenesis and prevention of osteonecrosis. Dexamethasone, a type of glucocorticoids (GCs), induce apoptosis of osteoblasts and lead to the occurrence of non-traumatic osteonecrosis. This study aimed to explore the effects of different doses and duration of Dexamethasone on osteoblast apoptosis of rats in vitro.

Methods: Proliferation and apoptosis of osteoblasts after Dexamethasone treatment were detected using cell counting kit-8 (CCK-8) assay and FITC-Annexin V/PI staining. The expressions of caspase-3 and -9 in osteoblasts after Dexamethasone treatment were analyzed using western blotting and qRT-PCR. Dexamethasone remarkably inhibited proliferation and induced apoptosis of osteoblasts in a dose-and duration-dependent manner.

Results: As the intervention time extended, the expression of caspase-3 mRNA and caspase-9 mRNA in different Dexamethasone groups gradually increased in a duration-dependent manner. With the same time of intervention (12h, 24h, 48h), the expression of caspase-3 and -9 mRNA gradually increased in a dose-dependent manner. After treated with 5 * 10-8M, 5 * 10-7M, 5 * 10-6M and 5 * 10-5M Dexamethasone for 24 hours, the expression of cleaved caspase-3 and -9 protein increased in a dose-dependent manner.

Conclusion: Dexamethasone can induce osteoblast apoptosis in a duration- and dose-dependent manner.

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