| 刘希光,张红军,宋婷婷,李敬东.凋亡素2配体对射线诱导的肺腺癌H1975细胞凋亡的影响[J].中华放射医学与防护杂志,2016,36(6):424-429 |
| 凋亡素2配体对射线诱导的肺腺癌H1975细胞凋亡的影响 |
| The effect of apoptosis-2 ligand on irradiation-induced apoptosis in lung adenocarcinima H1975 cells resistant to EGFR-TKI |
| 投稿时间：2015-09-03 |
| DOI：10.3760/cma.j.issn.0254-5098.2016.06.005 |
| 中文关键词: 凋亡素2配体 凋亡 辐射 H1975细胞系 |
| 英文关键词:Apoptosis-2 ligand Apoptosis Irradiation H1975 cell-line |
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| 中文摘要: |
| 目的 探讨凋亡素2配体(Apo-2L)对射线诱导的表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)耐药的肺腺癌H1975细胞凋亡作用的影响。方法 将肺腺癌H1975细胞分为空白对照组(未经任何处理)、药物组(凋亡素2配体组)、单纯照射组和药物联合照射组(凋亡素2配体+照射组),4组。同时,不同浓度的凋亡素2配体(200和228 ng/ml)作用于H1975细胞24 h后,均接受不同剂量的照射(照射剂量分别为1、1.5、2、2.5、3、3.5和4 Gy)。24 h后流式细胞仪检测各组细胞凋亡率。四甲基偶氮唑盐(MTT)法测定H1975细胞的抑制率。结果 MTT结果显示腺癌H1975抑制率随凋亡素2配体浓度增加而升高(χ2=136.17,P<0.05),凋亡率随凋亡素2配体浓度及照射剂量增加而增加(不同浓度t=5.12、6.38、7.89、9.27、11.77、14.12,P<0.05;不同剂量F=5.89、6.97,P<0.05)。放射增敏作用与放射剂量和药物浓度呈正比(不同浓度t=1.37、1.45、1.67、1.90、2.34、3.72,P<0.05;不同剂量F=26.74,P<0.05)。流式细胞仪检测各组的凋亡率,结果显示药物联合照射组凋亡率明显增加,差异有统计学意义(χ2=78.02,P<0.05)。结论 凋亡素2配体对体外培养的腺癌H1975细胞有抑制增殖和促进凋亡作用,且联合射线能明显提高腺癌H1975细胞的凋亡率。 |
| 英文摘要: |
| Objective To investigate whether the apoptosis-2 ligand (Apo-2L), known as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), could enhance irradiation-induced apoptosis in lung adenocarcinima H1975 cells that are resistant to the epithelial growth factor receptor (EGFR)-TKI. Methods Adenocarcinima H1975 cells were randomly divided into four groups:the control group, Apo-2L group, irradiation group, and both Apo-2L and irradiation group. H1975 cells were pretreated with Apo-2L under different concentrations of 200 and 228 ng/ml at 24 h before irradiation with doses of 1,1.5,2,2.5,3,3.5 and 4 Gy. The apoptosis rates of all groups were analyzed by flow cytometry 24 h post-irradiation. The inhibition rates of cell proliferation were measured by the MTT assay. Results MTT assay showed that the Apo-2L treatment significantly inhibited cell proliferation(χ2=136.17,P<0.05). The apoptosis rates of the four groups were different significantly, and the apoptosis rate of radiation combined with drug group was significantly higher than the other three groups(χ2=78.02,P<0.05). Conclusions The Apo-2L could not only inhibit the proliferation but also promote radiation-induced apoptosis of adenocarcinoma H1975 cells. |
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