研究了频率为1.43 MHz、强度为1 W/cm2的聚焦超声结合原卟啉Ⅸ对H-22肿瘤细胞的损伤作用，并探讨其生物学机制.应用台盼蓝拒染法检测不同处理后肿瘤细胞的存活率，环境扫描电镜和透射电镜观察细胞表面和内部的超微结构变化，荧光标记技术检测肿瘤细胞内活性氧的产生，硫代巴比妥酸（TBA）法检测肿瘤细胞脂质过氧化水平的变化.发现原卟啉Ⅸ-声动力学方法对H-22细胞产生的损伤效应表现为：细胞存活率明显下降，细胞表面和内部的超微结构改变，胞内活性氧和脂质过氧化水平增高.结果表明：原卟啉Ⅸ-声动力学方法能够使肿瘤细胞产生活性氧自由基，造成膜脂质过氧化，直接或间接地破坏细胞的膜系统，从而杀伤肿瘤细胞.

The damage of H-22 tumor cells induced by ultrasound activated protoporphyrin Ⅸ was investigated (1.43 MHz, 1 W/cm2). And the bio-mechanism of sonodynamic therapy (SDT) was also discussed. Trypan blue exclusion method was used to analyze the viability of H-22 cells. Scanning electronic microscope (SEM) and transmission electron microscope (TEM) were used to observe the ultrastructure of cell surface and interior. The production of reactive oxygen species (ROS) was assayed by fluorescence labeling technique, and the thiobarbituric acid (TBA) method was used to measure the lipid peroxidation levels. The results indicated that the membrane system of tumor cell was damaged and PPⅨ-sonodynamic therapy could induce the tumor cell to produce ROS which damaged the membrane of cell and induced lipid peroxidation. These results imply that PPⅨ-sonodynamic therapy has the significant damage effects on H-22 tumor cells and the lipid peroxidation could be increased by ROS. Based on these results mentioned above, PPⅨ-sonodynamic therapy can kill tumor cells through its direct and indirect effects on the membrane system of cells.