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目的初步研究超声激活原卟啉IX(PPIX)对S180肿瘤细胞的杀伤作用,并探讨其作用的生物学机制。方法采用频率为2·2MHz,强度为3W/cm2的聚焦超声,结合120μmol/L的PPIX作用于S180肿瘤细胞,通过台盼蓝拒染法检测细胞的存活率;扫描电镜观察细胞膜表面超微结构变化;活性氧试剂盒检测细胞悬液中活性氧的生成量;酶化学方法检测细胞内几种抗氧化物酶活性的变化。结果同等条件下,超声结合PPⅨ对细胞的损伤显著高于单纯超声组,而单纯PPⅨ表现出无明显的细胞毒作用;酶化学方法显示,超声激活PPⅨ后细胞内的丙二醛(MDA)含量显著增加,而细胞内的抗氧化物酶类均有不同水平的下降,并且与处理后细胞悬液中活性氧的生成量相关。结论超声激活原卟啉Ⅸ产生的活性氧自由基作用于细胞膜,增加膜脂质过氧化水平,降低细胞内的抗氧化物酶的含量,可能是其损伤S180肿瘤细胞的主要因素之一。
Objective To study the cytotoxicity of ultrasound-activated protoporphyrin IX (PPIX) on S180 tumor cells and explore the biological mechanism of its action. Methods Focused ultrasound with a frequency of 2·2MHz and intensity of 3W/cm2 was used in combination with 120μmol/L PPIX to treat S180 tumor cells. The viability of the cells was detected by trypan blue exclusion; scanning electron microscopy was used to observe the ultrastructure of the cell membrane surface. Changes; Reactive oxygen species was used to detect the amount of reactive oxygen species in cell suspensions; Enzyme chemistry was used to detect changes in the activity of several antioxidant enzymes in cells. Results Under the same conditions, ultrasound-associated PPIX had significantly higher damage to cells than did ultrasound alone, but PPIX showed no obvious cytotoxicity; enzyme chemistry showed that intracellular malondialdehyde (MDA) content after ultrasound activation of PPIX. Significantly increased, but the level of antioxidant enzymes within the cell has a different level of decline, and is related to the amount of reactive oxygen species produced in the cell suspension after treatment. Conclusion The activation of active oxygen free radicals produced by ultrasound porphyrin IX on the cell membrane, increase of membrane lipid peroxidation, and reduction of intracellular antioxidant enzyme content may be one of the main factors that damage the S180 tumor cells.