Research Article

EF24 Suppresses Cholangiocellular Carcinoma Progression, Inhibits STAT3 Phosphorylation, and Induces Apoptosis via ROS-Mediated Oxidative Stress

Figure 3

EF24 treatment leads to excessive intracellular ROS production and depletion of total glutathione levels in SNU478 and HuCC-T1 CCC cells. (a) EF24 significantly increased ROS as well as superoxide levels as shown using flow cytometry. This effect, however, was reverted in the presence of the antioxidant N-acetyl cysteine (NAC). (b) EF24 also depleted global glutathione (GSH) levels in both SNU478 and HuCC-T1 cells, whereas in the presence of NAC, GSH levels remained unaffected and were found to be comparable to those found in mock-treated controls using a colorimetric assay (“ns” indicates p>0.05; “” indicates p<0.001).
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