| 乔俏,姜元军,李光.NF-κB抑制与X射线诱导的人非霍奇金淋巴瘤细胞凋亡的研究[J].中华放射医学与防护杂志,2012,32(2):182-185 |
| NF-κB抑制与X射线诱导的人非霍奇金淋巴瘤细胞凋亡的研究 |
| Inhibition of NF-κB enhanced X-ray irradiation induced apoptosis in human non-Hodgkin lymphoma |
| 投稿时间：2011-07-17 |
| DOI：10.3760/cma.j.issn.0254-5098.2012.02.019 |
| 中文关键词: 淋巴瘤|NF-κB|X射线|Survivin|凋亡 |
| 英文关键词:Lymphoma|NF-κB|X-rays|Survivin|Apoptosis |
| 基金项目:辽宁省教育厅基金(2009A754) |
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| 中文摘要: |
| 目的 探讨NF-κB p65对X射线诱导人非霍奇金淋巴瘤(non-Hodgkin lymphoma, NHL)细胞凋亡的作用及其调控机制。方法 以NF-κB p65抑制剂quinazoline(QNZ)处理人NHL细胞。将NHL细胞株Namalwa、Ramos和 Raji细胞分为空白对照组、单纯照射组(IR)和X射线+QNZ实验组(IR+QNZ),采用Annexin-Ⅴ染色方法检测肿瘤细胞凋亡水平的变化,采用Western blot方法检测各细胞株中Survivin及凋亡相关蛋白Bax、Bcl-2和Cleaved Caspase-3的表达水平;应用实时定量PCR方法检测Survivin mRNA水平。结果 应用流式细胞仪检测凋亡细胞百分比,结果显示,QNZ处理后进行照射与单纯照射组相比凋亡细胞明显增加,且具有药物浓度依赖性(t=2.93~12.52, P<0.05),Western blot法检测结果显示,电离辐射可显著增加人NHL细胞中Survivin蛋白的表达。而应用1、10和50 nmol/L QNZ处理人NHL细胞24 h后进行照射,可显著下调电离辐射所诱导的NHL细胞中的Survivin蛋白表达。随药物浓度增加其作用更为明显(t=3.29~16.72,P<0.05)。同时凋亡相关蛋白Bcl-2表达减低,而Bax和Cleaved caspase-3蛋白表达增加,Bcl-2/Bax比值明显降低,与单纯照射组相比,差异有统计学意义(t=6.20~9.91, P<0.05)。预处理QNZ后射线诱导的3种NHL 细胞Survivin mRNA均不同程度下降。结论 抑制NF-κB能够增加X射线诱导的NHL细胞凋亡,其机制可能与下调Survivin蛋白表达水平及对凋亡相关蛋白Bcl-2家族的调节有关。 |
| 英文摘要: |
| Objective To investigate the role of NF-κB in radiation-induced apoptosis of human non-Hodgkin lymphoma (NHL) cells and the mechanism involved. Methods Three human non-Hodgkin lymphoma cell lines, Namalwa,Ramos, and Raji cells were divided into control, IR and IR+QNZ (10 nmol/L) groups,respectively. Annexin-Ⅴ kit was used to determine cell apoptosis. Protein expression levels of Survivin, Bax, Bcl-2 and cleaved Caspase-3 were evaluated by Western blot. Survivin mRNA was quantified by real-time PCR. Results Inhibition of NF-κB by QNZ pretreatment significantly enhanced X-ray induced apoptosis in human NHL cells in a dose-dependent manner (t=2.93-12.52, P<0.05). At the same time, QNZ significantly reversed the expression levels of Survivin protein and mRNA that were up-regulated by radiation(t=3.29-16.72,P<0.05). QNZ also increased the levels of Caspase-3 and pro-apoptotic protein Bax, but reduced anti-apoptotic protein Bcl-2 expression level and hence the ratio of Bcl-2/Bax. Conclusions Inhibition of NF-κB could enhance radiation-induced cell apoptosis in human NHL cells through down-regulating Survivin expression and decreasing Bcl-2/Bax ratio. |
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