| 山枫,朱杰,文军,等.地塞米松通过抑制 p53蛋白降解诱导成骨细胞凋亡[J].安徽医药,2023,27(5):888-893. |
| 地塞米松通过抑制 p53蛋白降解诱导成骨细胞凋亡 |
| Dexamethasone induces apoptosis in osteoblast cells by inhibiting p53 protein degradation |
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| DOI：10.3969/j.issn.1009-6469.2023.05.009 |
| 中文关键词: 地塞米松 细胞凋亡 成骨细胞 p53 成骨 |
| 英文关键词: Dexamethasone Apoptosis Osteoblast P53 Osteogenesis |
| 基金项目:国家自然科学基金资助项目( 82172520) |
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| 摘要点击次数: 1970 |
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| 中文摘要: |
| 目的观察地塞米松对成骨细胞凋亡的影响并探讨其作用机制。方法分别采 CellTiter-Glo.荧光细胞活力检测试剂盒和 Annexin V-FITC/PI双染凋亡检测试剂盒测定地塞米松作用后 MC3T3-E1细胞的增殖和凋亡。蛋白质印迹法( Western blotting)检测地塞米松作用后 MC3T3-E1细胞和 hFOB1.19细胞胱天蛋白酶 3(caspase-3)/裂解 caspase-3和 PARP/裂解 PARP的表达。用 Western blotting和 PCR分析地塞米松作用后 MC3T3-E1细胞中 p53和检控点激酶 2(Chk2)的表达。探讨 p53敲除和 Chk2敲除在地塞米松诱导 MC3T3-E1细胞凋亡中的作用。结果地塞米松能显著抑制 MC3T3-E1细胞的生长并诱导其凋亡。地塞米松能通过促进 p53的表达诱导成骨细胞凋亡。地塞米松对 P53蛋白表达的调节作用是通过上调 Chk2来实现的， Chk2与 P53相互作用，抑制 P53蛋白的降解。 P53基因敲除可通过降低裂解 caspase-3和裂解 PARP的表达来抑制地塞米松诱导的 MC3T3-E1细胞凋亡，经 Dex处理的 MC3T3-E1和 hFOB1.19细胞中 Ceaved PARP(0.38±0.02比 0.20±0.01、0.29±0.02比 0.20± |
| 英文摘要: |
| Objective To observe the effect of dexamethasone on the apoptosis of osteoblasts and explore its mechanism.Methods The cell proliferation and apoptosis of MC3T3-E1 cells after Dex treatment were determined by the CellTiter-Glo. Luminescent Cell Viability Assay kit and Annexin V-FITC/PI Double Staining Apoptosis Detection Kit, respectively. The expressions of caspase-3/ Cleaved-caspase-3 and PARP/Cleaved-PARP in MC3T3-E1 cells and hFOB1.19 cells after Dex treatment were determined by western blotting. The expressions of p53 and Chk2 in MC3T3-E1 cells after Dex treatment were analyzed by western blotting and qRT-PCR. The effects of p53 knockdown and Chk2 knockdown on Dex-induced apoptosis of MC3T3-E1 cells were explored.Results Dex can re-markably inhibit cell growth and induce apoptosis of MC3T3-E1 cells. Dex induced osteoblast apoptosis by promoting p53 expression.The regulatory effect of Dex on p53 expression is mediated by its upregulation of Chk2, which interacted with p53 and inhibited p53protein degradation. Knockdown of p53 alleviated Dex-induced MC3T3-E1 cell apoptosis by decreasing the expressions of cleaved-cas-pase 3 and Cleaved PARP(0.38±0.02 vs. 0.20±0.01, 0.29±0.02 vs. 0.20±0.02).Conclusion Dex increased Chk2 protein expression, which stabilizes the protein expression of p53, in turn promoting osteoblasts apoptosis. |
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