低温等离子体对不同恶性肿瘤细胞的杀伤作用及其机制研究

目的探讨低温等离子体(LTP)对人肝癌细胞株HepG2、非小细胞肺癌细胞株A549和人子宫颈癌细胞株HeLa的杀伤作用及其可能作用机制。方法采用四甲基偶氮唑蓝法测定LTP对人肝癌细胞株HepG2、非小细胞肺癌细胞株A549和人子宫颈癌细胞株HeLa的增殖抑制作用,透射电子显微镜下观察LTP对HepG2细胞、A549细胞和HeLa细胞的超微结构改变的作用,Muse细胞分析仪检测细胞凋亡,Westernblot检测凋亡相关蛋白的变化。结果HepG2细胞、HeLa细胞和A549细胞存活率为50%时,LTP的照射时间分别为107、121和127s。LTP对HepG2细胞、A549细胞和HeLa细胞的超...

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Published in中华肿瘤杂志 Vol. 38; no. 10; pp. 725 - 730
Main Author 王利利 秦颂兵 徐晓婷 胡超 钱丹琪 叶超 周菊英
Format Journal Article
LanguageChinese
Published 215006,苏州大学附属第一医院放疗科%215006,苏州大学物理与光电能源学部 2016
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Summary:目的探讨低温等离子体(LTP)对人肝癌细胞株HepG2、非小细胞肺癌细胞株A549和人子宫颈癌细胞株HeLa的杀伤作用及其可能作用机制。方法采用四甲基偶氮唑蓝法测定LTP对人肝癌细胞株HepG2、非小细胞肺癌细胞株A549和人子宫颈癌细胞株HeLa的增殖抑制作用,透射电子显微镜下观察LTP对HepG2细胞、A549细胞和HeLa细胞的超微结构改变的作用,Muse细胞分析仪检测细胞凋亡,Westernblot检测凋亡相关蛋白的变化。结果HepG2细胞、HeLa细胞和A549细胞存活率为50%时,LTP的照射时间分别为107、121和127s。LTP对HepG2细胞、A549细胞和HeLa细胞的超微结构均有不同程度的破坏,表现为细胞核和细胞器碎裂。HepG2细胞、A549细胞和HeLa细胞经LTP处理(处理时间为细胞存活率为50%时照射时间的1/6)后24h,与对照组比较,凋亡率增加(P〈0.05)。Westernblot检测结果显示,抗凋亡蛋白Bcl一2蛋白表达下调,促凋亡蛋白Bax蛋白的表达增高,DNA修复蛋白x线修复交错互补基因1蛋白表达下调。结论LTP对HepG2细胞株、A549细胞株和HeLa细胞株均有明显的杀伤作用,可能与诱导细胞凋亡和抑制DNA修复有关。
Bibliography:Deparment of Radiation Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China ( Wang LL, Qin SB, Xu XT, Hu C, Qian DQ, Zhou JY) ; Department of Physics, Optoelectronics and Energy, Soochow University, Suzhou 215006, China ( Ye C)
Objective To investigate the killing effect of low-temperature plasma (LTP) on HepG2, A549 and HeLa cell lines and explore its possible mechanism. Methods The inhibitory effect of LTP on the proliferation of HepG2, A549 and HeLa cells was determined by MTI" assay. Transmission electron microscopy was used to observe the ultrastructural changes of HepG2, A549 and HeLa cells treated with LTP. Cell apoptosis was detected by Muse cytometry. Western blot was used to detect the expression of apoptosis-related proteins. Results The survival rates of LTP-irradiated HepG2 cells (irradiated for 107 s), HeLa cells (irradiated for 121 s) and A549 cells (irradiated for 127 s) were 50%. LTP destroyed the ultrastructure of HepG2, A549 and HeLa cells to different degrees,
ISSN:0253-3766
DOI:10.3760/cma.j.issn.0253-3766.2016.10.002