Research Paper Volume 16, Issue 10 pp 9264—9279
Bufotalin enhances apoptosis and TMZ chemosensitivity of glioblastoma cells by promoting mitochondrial dysfunction via AKT signaling pathway
Figure 5. Bufotalin promoted mitochondrial dysfunction by increasing ROS and decreasing the phosphorylation of AKT. (A, B) ROS quantification was determined by flow cytometry using the H2DCFDA. (C, D) mitoROS quantification was determined by flow cytometry using the MitoSox. (E, F) Mitochondrial morphology was determined by Mito tracker using the confocal. (G, H) Decrease in ATP levels with increasing bufotalin concentration. (I, J) The expression levels of Bcl2, BAD, AKT and p-AKT were analyzed by western blot. Data are the mean ± SD of triplicate samples. Significant differences compared with the control are indicated by *p < 0.05, **p < 0.01, and ***p < 0.001.