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三氧化二砷对人胃腺癌细胞株SGC-7901细胞核及线粒体作用的实验研究

The effect of arsenic trioxide on nuclei and mitochondria of gastric adenocarcinoma cells SGC-7901

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【作者】 史兴晔王恂薛东波潘尚哈郑彪李玉丹张伟辉

【Author】 SHI Xing-ye, WANG Xun, XUE Dong-bo, PAN Shang-ha, ZHENG Biao, LI Yu-dan, ZHANG Wei-hu (First Clinical College of Harbin Medical University, Harbin150001, Heilongjiang, China)

【机构】 哈尔滨医科大学附属第一临床医学院

【摘要】 目的:研究三氧化二砷(As2O3)对人胃腺癌细胞株SGC-7901的生物效应及其对线粒体和半胱氨酸蛋白酶家族-3(caspase-3)的作用。方法:通过MTT比色实验检测不同浓度As2O3对该细胞株的生长抑制作用;经Hoechst 33258染色后用荧光显微镜观察细胞核的形态变化;经过细胞线粒体膜电位检测区分凋亡细胞与正常细胞,并经流式细胞仪分析;caspase-3吸光度检测法测定As2O3组caspase-3的活化程度。结果:As2O3明显抑制SGC-7901人胃腺癌细胞的生长,抑制作用的强度呈时间依赖性(方差分析,P<0.01);Hoechst 33258染色后荧光显微镜观察细胞核固缩碎裂边集呈强蓝色荧光;线粒体膜电位检测法,流式细胞仪检测法,caspase-3吸光度检测法均检测到胃腺癌细胞的凋亡。结论:As2O3破坏线粒体跨膜电位和激活caspase-3活性可能是As2O3诱导人胃腺癌SGC-7901细胞凋亡的重要机制。

【Abstract】 Objective:To explore the biological effect of arsenic trioxide (As2O3) in inhibition of proliferation of gastric adenocarcinoma cells SGC-7901 and.To investigate the effect of As2O3 to mitochondria and caspase-3 of the human gastric adenocarcinoma cells SGC-7901.Methods:The inhibition of proliferation of SGC-7901 cells treated with As2O3 was studied in growth curve and MTT assay.The nuclei were stained by Hoechst 33258, the nuclearmorphologic changes were observed by fluorescence microscope and apoptosis index was calculated.The apoptosis of SGC-7901 cells induced by As2O3 was investigated through method of detecting mitochondrial transmembrane potential, flow cytometry and detecting caspase-3.Results:As2O3 can inhibit significantly the growth of SGC-7901.SGC-7901 cells treated by As2O3 exhibited morphologic features of apoptosis, including nuclear shrinkage, nuclearcondensation, nuclear fragmentation and formation of apoptotic bodies.A typical apoptosis of SGC-7901 cells treated by As2O3 was detected by method of detecting mitochondrial transmembrane potential, flow cytometry and detecting caspase-3.Conclusion:As2O3 can induce significantly apoptosis of gastric cancer cells SGC-7901.The apoptosis induced by As2O3 was associated closely with the disruption of mitochondrial transmembrane potential and activation of caspase-3.

【基金】 国家自然科学基金面上项目(30972907)
  • 【文献出处】 现代生物医学进展 ,Progress in Modern Biomedicine , 编辑部邮箱 ,2010年15期
  • 【分类号】R735.2
  • 【被引频次】1
  • 【下载频次】88
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