Relationship between the level of Bax-Bcl-2 heterodimer and apoptosis of gastric cancer cells

Objective:To elucidate the relationship between Bax/Bcl-2 heterodimer and apoptosis of gastric cancer cells in- duced by non-steroidal anti-inflammatory drugs (NSAIDs).Methods:Apoptosis was induced by NSAIDs and determined by acri- dine orange (AO) staining,laser confocal laser scanning microscopy,flow cytometry,and TdT-mediated dUTP nick end labeling assay.The expression of Bax and Bcl-2 protein was detected by Western blot.The level of Bax-Bcl-2 heterodimer was deter- mined by immuno-precipitation/Western blot (Ip-Wb) analysis.Results:Apoptosis of AGS cells were induced after 24-h treat- ment with indomethacin 800 mmol/L or aspirin 8 mmol/L.The apoptotic rate induced by indomethacin was (9.34±1.99)% at 24 h and (38.97±3.36)% at 48 h.The apoptotic rate induced by aspirin was (17.60±3.30)% at 48 h.The level of Bax-Bcl- 2 heterodimer gradually increased from 6 h to 48 h in a time-dependent manner.The increase in Bax protein was significant dur- ing 6-24 h.But the expression of Bcl-2 protein was undetected.Condusion:NSAIDs could induce apoptosis of AGS cells.Bax/ Bcl-2 heterodimer might promote the apoptosis and serve as an important target for NSAIDs to regulate apoptosis.