Effects of eicosapentaenoic acid on apoptosis and mitochondria in HepG2 cells
Chun Wang
Abstract
Chun Wang
Abstract
AIM: To investigate the mitochondria changes in human hepatoblastoma G2 (HepG2) cell apoptosis induced by eicosapentaenoic acid (EPA). METHODS: In the HepG2 cells incubated with EPA in vitro, cell apoptosis was detected by DNA Ladder, the changes of mitochondria function and quantity were determined with methyl thiazolyl tetrazolium (MTT) colorimetric assay and fluorescence probe. The expression and activity of Caspase-9 were measured in HepG2 cell apoptosis with Western blotting and special substrate. RESULTS: Twenty-four hours after exposure to 120 μmol/L EPA, HepG2 cells displayed the apoptosis by the DNA ladder pattern; the number of the mitochondria was decreased; the A value by the MTT test was 0.173± 0.065, which indicated that the function of mitochondria was significantly declined (P0.01); compared with the untreated HepG2 cells, the expression of Caspase-9 was up-regulated and the activity of Caspase-9 was increased to 75.4±4.8 in HepG2 cells treated with EPA (P0.01). CONCLUSION: The changes of mitochondria may play a great role in the HepG2 cell apoptosis induced by EPA.
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AIM: To investigate the mitochondria changes in human hepatoblastoma G2 (HepG2) cell apoptosis induced by eicosapentaenoic acid (EPA). METHODS: In the HepG2 cells incubated with EPA in vitro, cell apoptosis was detected by DNA Ladder, the changes of mitochondria function and quantity were determined with methyl thiazolyl tetrazolium (MTT) colorimetric assay and fluorescence probe. The expression and activity of Caspase-9 were measured in HepG2 cell apoptosis with Western blotting and special substrate. RESULTS: Twenty-four hours after exposure to 120 μmol/L EPA, HepG2 cells displayed the apoptosis by the DNA ladder pattern; the number of the mitochondria was decreased; the A value by the MTT test was 0.173± 0.065, which indicated that the function of mitochondria was significantly declined (P0.01); compared with the untreated HepG2 cells, the expression of Caspase-9 was up-regulated and the activity of Caspase-9 was increased to 75.4±4.8 in HepG2 cells treated with EPA (P0.01). CONCLUSION: The changes of mitochondria may play a great role in the HepG2 cell apoptosis induced by EPA.
Key concepts: Apoptosis, Mitochondrion, Eicosapentaenoic acid, Molecular biology, Hepatoblastoma, Cell, Blot, MTT assay