Objective       To determine the effects of photodynamic therapy (PDT) with aloe emodin (AE) as photosensitizer on the proliferation and apoptosis in breast cancer cells and investigate the underlying mechanism.       Methods       After breast cancer cell line MCF-7 were treated with AE-induced PDT

cell proliferation was measured by CCK-8 assay. Cellu

lar apoptosis was detected by Hoechst nuclear staining and flow cytometry. The level of reactive oxygen species (ROS) were observed by DCFH-DA staining. Mitochondrial membrane potential was tested by JC-1 staining. The expression of Caspase-3 and Bcl-2 was assessed by Western blotting.       Results       Cell proliferation was significantly suppressed in the MCF-7 cells after AE-PDT in a dose-dependent manner (P0.05). AE-PDT resulted in remarkable increased apoptotic rate and secondary necrotic rate in the cells compared with the photodynamic therapy cells

AE treated cells

and normal control cells (P0.05)

and there was no difference among the latter 3 groups (P0.05). After the cells were treated by an energy density of 12 J/cm

2

(drug density 10 μmol/L

optical power density 40 mW/cm

2

for 300 s). Hoechst33342 staining displayed karyopyknosis

fragmentation

apoptotic bodies

DCFH-DA staining showed increased level of ROS

and JC-1 staining suggested decreased mitochondrial membrane potential

and Western blot analysis found that the protein level of Caspase-3 was increased and that of Bcl-2 decreased.       Conclusion       PDT with AE as photosensitizer significantly inhibits the proliferation and induces apoptosis in breast cancer MCF-7 cells. The mitochondrial pathway is involved in the AE-mediated PDT-induced apoptosis.