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Objective: To investigate the apoptosis effect of TNF-α on HepG2 cells and its mechanism in vitro. Methods: HepG2 cells were treated with TNF-α (400 U/mL). HepG2 cells treated with TNF-α for 24 h and apoptosis was proved by DNA fragments on gel electrophoresis. Fluorescent quantitative real-time PCR was used to detect Fas and FasL expression. HepG2 cells treated by TNF-α were co-cultivated with normal HepG2 cells. Apoptosis of HepG2 cells was determined by the method of FACS. Results: After 24 h TNF-α treatment, DNA was collapsed into fragments to form DNA ladder in gel elec- trophoresis; FasL expression increases and induces HepG2 cells apoptosis. By FACS, 98.4% of the co-cultivated cells were apoptosis, but 16.5% cells in control group were apoptosis. Conclusion: TNF-α can induce apoptosis of HepG2 cells in vitro. FasL expression on TNF-α pre-treated HepG2 cells increased and these cells can lead normal HepG2 cells to apoptosis. This may attribute to the cure of virus hepatitis and hepatoma.
Objective: To investigate the apoptosis effect of TNF-α on HepG2 cells and its mechanism in vitro. Methods: HepG2 cells were treated with TNF-α (400 U / mL) proved by DNA fragments on gel electrophoresis. Fluorescent quantitative real-time PCR was used to detect Fas and FasL expression. HepG2 cells treated by TNF-α were co-cultivated with normal HepG2 cells. Apoptosis of HepG2 cells was determined by the method of FACS Results: After 24 h TNF-α treatment, DNA was collapsed into fragments to form DNA ladder in gel elec- trophoresis; FasL expression increases and induces HepG2 cells apoptosis. By FACS, 98.4% of the co-cultivated cells were apoptosis, but 16.5% cells in control group were apoptosis. TNF-α can induce apoptosis of HepG2 cells in vitro. FasL expression on TNF-α pre-treated HepG2 cells increased and these cells can lead normal HepG2 cells to apoptosis. This may attribute to the cure of virus hepatiti s and hepatoma.