Figure 6.

APAP-induced HepG2 cell death. (A,B) Dose dependence of viabilities of HepG2 cell treated with APAP (A) or H₂O₂ (B) for 24 h. Cell viability is presented as percentage of viable cells in trypan blue exclusion assay. (C) HepG2 cell death upon exposure to 20 mM APAP or 1 mM H₂O₂ for 24 h. Hoechst33342- and propidium iodide (PI)-staining were visualized by fluorescence microscopy. Scale bar, 100 μm. (D,E) DNA fragmentation in HepG2 cells. Cells were exposed for 24 h to APAP (D) (5, 15, and 20 mM) or H₂O₂ (E) (250 μM, 500 μM, and 1 mM). M is the DNA marker. (F) Caspase 3/7 activity in HepG2 cells stimulated with 20 mM APAP or 1 mM H₂O₂ for 24 h. (G) Effects of either Ca²⁺-calmodulin antagonist (W-7; 1 μM), cyclosporine A (CsA; 4 μM), or different MAPK-specific inhibitors (U0126, SP600125 and SB203580; 20 μM) on HepG2 cell death induced by APAP for 24 h in Hoechst33342- and PI-staining assays. Data points are mean ± SEM. P≥0.05, ^*P < 0.05, ^**P < 0.01, and ^***P < 0.001 compared to DMSO or control. Differences not statistically significant are labeled as (ns). All data were analyzed by ANOVA and Bonferroni post-hoc.