The Therapeutic Potential of Aprepitant in Glioblastoma Cancer Cells through Redox Modification

Figure 6

Schematic presentation. Once SP binds to NK1R, the intracellular levels of MDA and ROS increase in glioblastoma-derived U87 cells, which in turn through disturbing the antioxidant system reinforce the survival and the proliferative capacity of neoplastic cells. Aprepitant, an antagonist of NK1R, on the other hand, prevents the oncogenic activity of SP. This agent abrogates the activity of MDA and subsequently the production of ROS within the malignant cells. Moreover, through potentiating the activity of the antioxidant system, as revealed by the elevation in the activity of thiol and TAC, aprepitant decreases the metabolic activity of U98 cells.