| 刘莉,陆海,CE.Ruebe,Ch.Ruebe.人非小细胞肺癌细胞受照射后肿瘤坏死因子水平的变化[J].中华放射医学与防护杂志,2004,24(4):313-316 |
| 人非小细胞肺癌细胞受照射后肿瘤坏死因子水平的变化 |
| Regulation of TNF-α level after irradiation of human NSCLC cell lines in vitro |
| 投稿时间：2003-12-16 |
| DOI： |
| 中文关键词: 非小细胞肺癌细胞系(A549,NCI-H596) 肿瘤坏死因子 放射治疗 |
| 英文关键词:Non-small cell lung cancer cell lines(A549,NCl-H596) Tumor necrosis factor(TNF-α) Ionizing radiation |
| 基金项目:国家留学基金资助项目(20842007) |
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| 中文摘要: |
| 目的 观察非小细胞肺癌(NSCLC)细胞系A549和NCIH596受X射线照射后肿瘤坏死因子(TNFα)mRNA表达及其蛋白水平的变化。方法 应用实时荧光RTPCR技术,观察肺癌细胞系A549和NCIH596照射2、5、10、20、30和40Gy后1、3、6、12、24、48和72hTNFαmRNA表达及其蛋白水平。应用免疫组织化学法(ELISA)检测相应培养液中TNFα蛋白的水平。同时进行集落形成实验观察2种细胞系的放射敏感性。结果 X射线照射后TNFαmRNA表达及其蛋白水平较照射前升高,吸收剂量达40Gy时TNFαmRNA表达水平达高峰,为对照组的83倍。NCIH596细胞受照射后1hTNFαmRNA表达逐渐升高,6h达高峰,为对照组的568倍。NCIH596细胞受照射后TNFα蛋白水平逐渐升高,受照射后24h达高峰(为基础水平的58倍)。且与受照射剂量有关。A549细胞受照射后1hTNFαmRNA表达仅见瞬间升高,随后即降至基础水平。而且,A549细胞受照射后TNFα蛋白水平无明显升高。结论 X射线可诱导NSCLC细胞系NCIH596产生TNFα,呈现时间、剂量依赖性改变。 |
| 英文摘要: |
| Objective Even though radiotherapy plays a major role in the local treatment of non-small cell lung cancer(NSCLC), little is known about the molecular effects of irradiation on this tumor.In the present study, we examined two NSCLC cell lines for their TNF-α production after irradiation. Methods Two human NSCLC cell lines(A549:squamous;NCl-H596:adenosquamous)were investigated for their TNF-α mRNA(real-time RT-PCR)and TNF-α protein expressions(ELISA) after exposure to different irradiation doses(2, 5, 10, 20, 30, 40 Gy) and time intervals(1, 3, 6, 12, 24, 48 or 72 h).The clonogenic survival was evaluated after irradiation with 2, 4, 6 and 8 Gy. Results Non-irradiated NSCLC cells exhibited no or very low TNF-α expression.For the NCl-H596 cell line, TNF-α expression was significantly elevated at 1-12 h(maximum 6 h:568-fold increase relative to unirradiated cells), and TNF-α protein production at 6-72 h post-irradiation(maximum 24 h:58-fold increase).The radiation-induced increase could already be observed after irradiation with 2 Gy.In contrast, A549 cells showed no irradiation-induced TNF-α production.The clonogenic survival of these cell lines was nearly indentical. Conclusion NCl-H596 cells produce significant quantities of TNF-α following irradiation in time-and dose-dependent manner.The pro-inflammatory cytokine TNF-α is a key mediator for the pathogenesis of radiation pneumonitis.Radiation-induced endogenous TNF-α expression in NSCLC cells may affect the normal lung tissue adjacent to the tumor and may be associated with an adverse clinical outcome of the patient. |
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