中文摘要：

目的探讨STAT3RNA干扰（RNAi）对脑胶质瘤U251细胞活性氧含量及DNA损伤的影响。方法利用构建好的STAT3RNAi载体（pSilencer2．1-STAT3，STAT3组）和pSilencer2．1-GFP（RNAi对照组）分别转染U251细胞，分别检测24、48和72h后细胞内活性氧（ROS）和丙二醛（MDA）水平；同时利用单细胞凝胶电泳方法，检测6、12和24h后细胞内DNA损伤；利用碘化丙啶（PI）单染流式检测12、24、36和48h后细胞周期分布情况。结果U251细胞转染pSilencer2．1-STAT324h后，细胞内ROS水平是对照的8．91倍（F=89．296，P〈0．05），48h后回复到正常水平；24、48和72hsiSTAT3组和siGFP组之间MDA水平无显著变化；同时，与出现明显拖尾现象的8Gy照射U251细胞阳性对照组相比，转染pSilencer2．1-STAT36h后部分细胞出现拖尾现象，12h后拖尾变得较少，24h后完全消失。与对照组相比，siSTAT3转染组12h后s期的滞后率是17．22％，G2／M的滞后率是6．4％；24h后G0／G1的滞后率是18．44％；36h后，S期的滞后率是17．99％。结论对U251细胞STAT3RNAi后，细胞内氧化还原状态发生改变，同时伴有DNA的损伤与修复。

英文摘要：

Objective To investigate the effects of signal transducer and activator of transcription 3 （STAT3） RNAi on the content of reactive oxygen species （ROS） and the DNA damage in glioma cells. Methods G]ioma cells of the line U251 ceils were cultured and transfected with STAT3 RNAi plasmid （pSilencer2. 1-STAT3, STAT3 group） and pSilcncer2. 1-GFP （GFP control group） respectively. Part of the U251 cells were irradiated with γ-rays of 60Co as positive control group of smear phenomenon. The levels of ROS and malondialdehyde （MDA） in the ceils were detected 24, 48, and 72 h later by flow cytometry and fluorescence chamolumineseence analyzer, respectively. The DNA damage in the transfected U251 cells was examined by using single cell gel electrophoresis assay, and the cell cycle distribution was examined using FACS PI staining 12, 24, and 36 h later. Results At 24 h after the transfection, the ROS level of the siSTAT3-transfected cells was 8.91 times that of the control group （ F = 89. 296, P 〈 0. 05 ） , and returned to the normal level 48 h later. There were not significant differences in the MDA level of the cells 24, 48, and 72 h later between the siSTAT3 group and siGFP group. Compared with the 8 Gy irradiation positive group with obvious smear phenomenon, smear phenomenon was shown in part of the cells in the siSTAT3 group 6 h later, became less 12 h later, and disappeared completely 24 h later. Compared with the control group, lag of S stage rate was 17.22% and the lag of G2/M stage rate was 6. 4% 12 h later in the siSTAT-transfected group, and the G0/G1 stage lag rate was 18.44% 24 h later, and the lag of S stage rate was 17.99% 36 h later. Conclusions Inhibition of STAT3 results in the change of oxidoreduction status in glioma cells, as well as damage and reparation of DNA.