Fig. 5: Investigation of anticancer mechanism for TBmA-Glu.
a Intracellular ROS generation in HepG2 cells PDT treatment groups, DCFH-DA (10 μM, 10 min) used as the indicator. DCF, λex = 488 nm, λem = 500 ± 20 nm. Scale bar, 20 μm. b The Clearance rates of different ROS scavengers (Trolox: 50 μM (ROO· scavenger); d-mannitol: 50 mM (·OH scavenger); Tiron: 10 mM (·O2– scavenger); NaN3: 5 mM (1O2 scavenger)) on the ROS induced by PDT of TBmA-Glu were evaluated. All assays (n = 3) were biologically independent samples, data expressed as average ± standard error. c Impact of TBmA-Glu (2 μM) on cellular GSSG/GSH ratios. All assays (n = 3) were biologically independent samples, data expressed as average ± standard error. Statistical significance: P values, ***P < 0.001, calculated with the one-sided Student’s t-test. d The expression levels of GGT and GPX4 in HepG2 cells of TBmA-Glu dark and PDT groups. Three independent experiments were performed. e The expression level of GGT1 in HepG2 cells in TBmA-Glu (2 μM) or 1% DMSO (Ctrl) for PDT groups. Three independent experiments were performed. Scale bar, 20 μm. f Transmission electron microscopy images revealed morphological changes in HepG2 cells treated with TBmA-Glu (2 μΜ, 24 h) without and under light irradiation conditions. Enlarged regions are indicated by red rectangles. Three independent experiments were performed. Scale bars represent lengths of 5  μm and 500 nm (for the enlarged images), respectively.
