论文部分内容阅读
目的:探讨冬凌草甲素诱导胰腺癌细胞株PANC-1凋亡的作用及其机制。方法:MTT法检测细胞存活率;Hoechst 33342染色后激光共聚焦显微镜观察细胞形态;PI染色后流式细胞术检测PANC-1细胞凋亡率;Western blotting检测JNK和p38 MAPK信号通路凋亡相关蛋白的表达。结果:冬凌草甲素作用PANC-1细胞24 h后,可浓度依赖性降低细胞存活率,IC50为49.80μmol/L。冬凌草甲素50、80μmol/L处理24 h后的PANC-1细胞可见典型的凋亡核改变,流式细胞仪分析细胞凋亡率明显增加。Western blotting结果证实80μmol/L冬凌草甲素可降低PANC-1细胞JNK、p38、Caspase-9、Caspase-3和PARP的蛋白表达,增加p-JNK、p-p38和活化的Caspase-9的蛋白表达。结论:冬凌草甲素可诱导胰腺癌PANC-1细胞凋亡,其机制与JNK和p38 MAPK信号转导通路凋亡相关蛋白的活化有关。
Objective: To investigate the effect of oridonin on apoptosis of pancreatic cancer cell line PANC-1 and its mechanism. Methods: The cell viability was detected by MTT assay. The morphological changes of cells were observed by laser scanning confocal microscope after Hoechst 33342 staining. The apoptosis rate of PANC-1 cells was detected by PI staining. The protein of JNK and p38 MAPK signal pathway expression. Results: After treated with oridonin for 24 h, PANC-1 cells could decrease the cell survival rate in a concentration-dependent manner with IC50 of 49.80 μmol / L. The apoptosis of PANC-1 cells treated with oridonin 50 and 80 μmol / L for 24 h showed typical apoptotic nuclear changes, and the apoptosis rate was significantly increased by flow cytometry. Western blotting confirmed that 80μmol / L oridonin could decrease the protein expression of JNK, p38, Caspase-9, Caspase-3 and PARP in PANC-1 cells and increase the expressions of p-JNK, p-p38 and activated Caspase-9 Protein. Conclusion: Rubescensine A can induce the apoptosis of pancreatic cancer PANC-1 cells, and its mechanism is related to the activation of apoptosis-related proteins of JNK and p38 MAPK signal transduction pathway.