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目的 :通过干扰体外培养的成骨样细胞 ,探索糖皮质激素所致成骨细胞凋亡的细胞分子机制。方法 :地塞米松诱导原代培养并传代的小鼠成骨样细胞 ,应用噻唑兰 (MTT)法检测细胞生存能力、流式细胞仪检测细胞凋亡、比色法检测半胱天冬酶Caspase 3的活性以及经EMSA检测NF κB活性。结果 :地塞米松使得成骨样细胞存活数量下降 ,Caspase 3活性升高并且NF κB活性下降。结论 :地塞米松对原代、未转化的成骨细胞有诱导凋亡的作用 ,这种作用是Caspase 3依赖性的 ,而NF κB似乎可以通过抑制Caspase 3保护细胞
OBJECTIVE: To explore the molecular mechanism of glucocorticoid-induced osteoblast apoptosis by interfering with osteoblast-like cells cultured in vitro. Methods: Primary cultured osteoblast-like cells were induced by dexamethasone. Cell viability was measured by MTT assay. Apoptosis was detected by flow cytometry. Caspase 3 activity and EMSA detection NF κB activity. RESULTS: Dexamethasone caused a decrease in the number of osteoblast-like cells, an increase in Caspase 3 activity, and a decrease in NF κB activity. CONCLUSIONS: Dexamethasone induces apoptosis in primary, untransformed osteoblasts, an effect that is Caspase 3-dependent, whereas NF-κB appears to protect cells by inhibiting Caspase 3