| ObjectiveTo investigate whether apigenin (API) induces apoptosis in human pancreaticcancer PANC-1cells and explore whether this mechanism is involved in depletion ofintracellular glutathione (GSH).MethodsHuman pancreatic cancer PANC-1cells cultured in vitro were treated with variousconcentration (20.0,40.0,80.0μmol/L) of API. The apoptotic rate (the percentage ofsub-G1cells) was determined by flow cytometry (FCM) using propidium iodide (PI)fluorescence staining. The histone/DNA fragment in pancreatic cancer PANC-1cellswas evaluated using enzyme linked immunosorbent assay (ELISA). The apoptoticeffect of morphology was observed by fluorescence microscope using Hoechst33258staining. The intracellular level of GSH was measured using spectrophotometer.ResultsFCM after PI staining showed that API (20.0,40.0,80.0μmol/L) significantlyincreased the apoptotic rate of human pancreatic cancer PANC-1cells (P＜0.05), ina concentration-dependent manner. ELISA showed that API (20.0,40.0,80.0μmol/L)in a concentration-dependently increased histone/DNA fragments in human pancreaticcancer PANC-1cells (P＜0.05). The typical morphological change of apoptosis,such as nuclear fragmentation, nuclear karyopycnosis, edge set of nuclearchromosomes, the formation of apoptotic bodies, were observed using fluorescence microscope after exposure of pancreatic cancer PANC-1cells to20.0,40.0,80.0μmol/L API for24h. API significantly reduced the intracellular level of GSH (P＜0.05) in human pancreatic cancer PANC-1cells (P＜0.05), in aconcentration-dependent manner. Importantly, the pretreated with500μmol/L GSHfor1h can effectively blocked the effects of API on induction of GSH depletion andapoptosis in pancreatic cancer PANC-1cells.Conclusion1. API possesses the effects of induction of apoptosis in human pancreatic cancerPANC-1cells in a concentration-dependent manner.2. The induction of apoptosis by API in human pancreatic cancer PANC-1cells wasassociated with depletion of intracellular GSH. |
PDF Full Text Request