Fig. 2.

PPC co-treatment induces oxidative stress and ferroptosis in gastric cancer cells. A-B KEGG and GO enrichment analyses of genes with significant differential expression between OXA+PPC and OXA-only treated cells, based on RNA-sequencing data. C ROS levels in gastric cancer cells post-treatment with or without PPC. Scale bar = 400 μm. D-G Evaluations of malondialdehyde (MDA) (D), superoxide dismutase (SOD) activity (E), glutathione (GSH) levels (F), and Fe²⁺ content (G) in gastric cancer cells treated with or without PPC. H-L Viability assessments of gastric cancer cells exposed to treatments with/without PPC for 24 h (H). Viability was also assessed in the presence of the ferroptosis inhibitor ferrostatin-1 (Fer-1; 2 μM) (I), the apoptosis inhibitor Z-VAD-FMK (50 μM) (J), the necroptosis inhibitor necrostatin (Nec-1; 50 μM) (K), and the antioxidant N-acetyl-l-cysteine (NAC; 5 mM) (L). Data are depicted as mean ± SD with significance indicators (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001).