论文部分内容阅读
研究癌光啉(PsD007)诱导的光动力疗法(PDT)对人喉癌细胞Hep-2的杀伤作用,初步探索其杀伤机制。用噻唑蓝(MTT)法测定在不同光敏剂浓度、光照剂量以及抗氧化剂作用下的PDT杀伤效果;用共聚焦显微镜观察光敏剂的亚细胞定位;用Annexin V/PI双染法检测凋亡率;用DCFH-DA探针检测活性氧(ROS)产量。MTT结果显示PDT对Hep-2的杀伤效果可高达85.4%,光敏剂浓度和能量密度都与细胞死亡率呈正相关;三种抗氧化剂均能不同程度拮抗PDT对细胞的杀伤效应,以叠氮钠效果最好;光敏剂主要定位在线粒体;PDT 2h后ROS产量是对照组的2.71倍;PDT 4h后凋亡率可达49.5%(能量密度为1.2J/cm2)和70.2%(能量密度为4.8J/cm2)。PsD007-PDT对Hep-2细胞有明显的杀伤作用,并可诱导细胞凋亡,线粒体可能是其起始靶点。
To study the killing effect of PDT induced by PsD007 on human laryngeal carcinoma cell line Hep-2 and its mechanism of killing. The killing effect of PDT under different photosensitizer concentrations, light doses and antioxidants was determined by MTT method. The subcellular localization of photosensitizer was observed by confocal microscopy. The apoptosis rate was detected by Annexin V / PI double staining ; DCFH-DA probe was used to detect the production of reactive oxygen species (ROS). MTT results showed that the killing effect of PDT on Hep-2 was as high as 85.4%. Both photosensitizer concentration and energy density were positively correlated with cell death rate. All three antioxidants could antagonize the cytotoxicity of PDT to varying degrees. Sodium azide The best photosensitizer was located in the mitochondria. After 2 hours of PDT, ROS production was 2.71 times that of the control group. After 4 hours of PDT, the apoptotic rate reached 49.5% (energy density 1.2J / cm2) and 70.2% (energy density 4.8 J / cm2). PsD007-PDT has a significant killing effect on Hep-2 cells and induces apoptosis. Mitochondria may be the initial target.