Figure 2.

Emodin inhibited cell proliferation and induced intrinsic apoptosis in Bel-7402 cells. (A) The chemical structure of emodin. (B) Bel-7402 cell viability after treatment with emodin determined by the MTT assay. (C) Apoptosis in emodin-treated Bel-7402 cells as assessed by flow cytometry. (D and E) The fluorescence images with JC-10 staining in Bel-7402 cells. Bel-7402 cells were exposed to emodin (100 μmol/L) for 24 h followed by 30-min incubation with JC-10. When the mitochondrial membrane potential (ΔΨm) was higher, the JC-10 accumulated in the mitochondria matrix to form the polymer producing red fluorescence; otherwise, the green fluorescence from the JC-10 monomers was used to represent the cells that lost ΔΨm. Quantitative data of the ratio of red and green fluorescence intensity were measured. (F and G) Expression level of intrinsic apoptosis-associated proteins was measured after emodin treatment by Western blotting analysis. Data were expressed as mean ± standard error of the mean. *P < 0.05, **P < 0.01, and ***P < 0.001 vs. ctrl group (0 μmol/L), respectively.