亚硒酸钠、砒霜对肺腺癌细胞周期、凋亡、耐药的影响

Effect of sodium selenite and white arsenic on cell cycle,Apoptosis,drug fast in adenocarcinoma of lung cell

目的通过比较低浓度亚硒酸钠、砒霜对肺腺癌细胞A549的周期、凋亡、耐药及线粒体的影响,探讨肺腺癌药物治疗的新方法。方法体外培养肺癌A549细胞,分为对照组及5.0μmol/L亚硒酸钠(A组)、5.0μmol/L砒霜(B组)处理组,药物处理24 h后以流式细胞仪检测细胞周期;Western blot检测三组促凋亡因子Caspase-3、抗耐药基因RARα的表达,RT-PCR检测三组凋亡抑制基因Bcl-2、细胞周期素CyclinD3表达;电子显微镜观察细胞线粒体结构与凋亡小体。结果与对照组相比,A、B组G0/G1期增加、S和G2/M期减少,出现细胞周期阻滞,凋亡细胞比例增加。Caspase-3、RARα表达上调,Bcl-2、cyclinD3表达下调。线粒体肿胀、线粒体嵴模糊不清,出现凋亡小体。结论亚硒酸钠、砒霜治疗肺腺癌均有良好的效果,因为氧化还原能力不同,作用各有侧重。

Objective To approach a new drug treatment of adenocarcinoma of lung, we compared the contribution of low concentration sodium selenite and white arsenic on cell cycle, Apoptosis, drug fast and mitochondria in adenocarcinoma of lung cell. Methods The cell A549 wss cultured and treated by 5.0μmol/L sodium selenite and white arsenic for 24 hour, respectively. The Flow cytometry was used to detect the cell cycle. The Western blot and RT-PCR method was used to detect the expression of caspase3, RARer, Bcl-2 and CyclinD3. The electronmicroscope was used to observe the change of mitochondria and apoptotic body. Results Compared with the control group, the proportion of G0/G1 phase and apoptosis cell increased, the proportion of S phase and G2/M plmse decreased, the cell cycle was arrested. The expression of Caspase-3 and RARer was up-regulated, the expression of Bcl-2 , CyclinD3 was down-regulated. The mitoehondria change to swell, the erlsta mioehondriales get unclear and the apoptotie body appeared. The effect of sodium selenite on changing drug fast was more significant, and so the effect of white arsenic on inducing Apoptosis and destroying the structure of mito ehondria. Conclusions The sodium selenite and white arsenic is effective on drug treatment in adenoearcinoma of lung cell, the contribution lays particular emphasis on different directions because of different oxidoreduetion capability, the oxydum of microelement is expected to be a new drug treatment of adenoearcinoma of lung.