茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.

Regulation of akt pathway in apoptosis of pancreatic cancer cells induced by polyphenols