Objective:The aim of the study was to determine the potential cytotoxicity and the underlying mechanism of emodin on HepG2 cells. Method:Am-blue assay were used to detect the toxicity of emodin on HepG2 cells. The level of intracellular reactive oxygen species (ROS) was detected by the DCFH-DA fluorescent dye

and the mitochondrial membrance potential was measured by the mitochondrial-specific lipophilic cationic fluorescent dye JC-1.The apoptotic cells were quantified by the Annexin V/PI double staining kit and analyzed by flow cytometry

and Western blot was used to detect the protein expression levels of cleaved Caspase-3

8

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cleaved-PARP

and other apoptosis-related proteins. Result:As compared with blank control group

emodin (15

30 μmol·L-1) had significant toxicity on HepG2 cells in a dose-and time-dependent manner (P<0.01)

promoted the production of intracellular ROS and reduced mitochondrial membrane potential (P<0.01). After treatment with emodin (15

30 μmol·L-1) for 24 h

the early apoptotic and late apoptotic cells were increased obviously (P<0.01). Further studies by Western blot indicated that emodin (15

30 μmol·L-1) exposure to HepG2 cells up-regulated the levels of cleaved Caspases-8

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3 and PARP in a dose-dependent manner (P<0.01). Conclusion:Emodin has a toxic effect on HepG2 cells

indicating that emodin has potential hepatotoxicity

and its toxic mechanism is via mitochondrial apoptotic pathway.