Aescin-induced reactive oxygen species play a pro-survival role in human cancer cells via ATM/AMPK/ULK1-mediated autophagy

摘要

Aescin induced apoptosis and activated autophagy in HepG2 and HCT 116 cells. , Aescin induced apoptosis in HepG2 and HCT 116 cells. Cells were treated with 0, 20, 40, 60 or 80 μg/mL aescin for 12 h. The apoptosis of HepG2 cells ( ) and HCT 116 cells ( ) was determined by flow cytometry (FCM). The experiment was performed in three independent studies. Quantitative analysis of apoptosis was performed. , Aescin activated autophagy in HepG2 and HCT 116 cells. Cells were treated with 0, 5, 10, 20, 40 or 60 μg/mL aescin for 12 h or treated with 40 μg/mL aescin for 0, 3, 6, 9, 12 or 24 h. The protein expression levels were determined. , Aescin-activated autophagy was independent of the mTOR pathway. The expression levels of proteins were determined in HepG2 cells and HCT 116 cells. β-Actin was used as a loading control. Quantitative analysis was performed with ImageJ. The values are means ± SD from three independent experiments. *  P P P P > 0.05 versus the control group