The aim of the present study was to investigate the effect of ZnPcS(2)P(2)-meditated sonodynamic
therapy (SDT) on U251 human
glioma cells and to identify its underlying biological mechanism. The growth inhibition rate was determined by MTT assay. The apoptotic rate was examined by flow cytometry. Fine structures were observed with transmission electron microscopy (TEM). Generation of
reactive oxygen species (ROS) was detected spectrophotometrically.
Caspase-3, -8 and -9 expression was detected by Western blot analysis. The growth inhibition rate of U251 human
glioma cells indicated that ZnPcS(2)P(2)-meditated SDT had a better growth inhibition rate of
tumor cells at a concentration of 5.0 μg/ml
ZnPcS(2)
P(2), at a 4-h incubation time with
ZnPcS(2)
P(2), and at 6 h re-incubation following SDT. At 6 h after SDT, the growth inhibition rate of cells was significantly higher compared to other groups, apoptosis could be detected in SDT by flow cytometry. TEM examination revealed morphological features of apoptosis or
necrosis. Furthermore,
caspase-3, -8 and -9 expression following SDT was found to be increased by Western blot analysis. Finally, generation of ROS in cells was also elevated. In conclusion, ZnPcS(2)P(2)-SDT is capable of inducing U251 cell apoptosis or
necrosis and has satisfying antitumor effects. The mechanism of ZnPcS(2)P(2)-meditated SDT involves ROS generation in U251 cells, which initiates subsequent apoptosis through the mitochondrial and
death receptor pathways.