冬凌草甲素通过内质网应激诱导胰腺癌细胞凋亡的研究

目的 探讨冬凌草甲素通过内质网应激诱导胰腺癌细胞凋亡的机制。方法 选取胰腺癌SW1990和Panc-1细胞株作为研究对象。采用细胞计数试剂-8(cell counting kit-8,CCK-8)和流式细胞术分别检测细胞增殖和凋亡情况，蛋白印迹法检测内质网应激相关因子葡萄糖调节蛋白78(glucose regulated protein 78 kD,GRP78)、环磷酸腺苷反应元件结合转录因子同源蛋白（C/EBP-homologous protein,CHOP）、裂解的天冬氨酸特异性半胱氨酸蛋白水解酶-12(cleaved cystein aspartate specific proteinase-12,cleaved Caspase-12)、活化的（active）Caspase-3、cleaved Caspase-3、cleaved多腺苷二磷酸多聚酶[poly(ADP-ribose) polymerase,PARP]的蛋白表达水平，实时荧光定量RCR检测GRP78、CHOP、Caspase-12的m RNA表达水平。结果 冬凌草甲素浓度和时间相关性抑制SW1990和Panc-1细胞增...

Study on apoptosis of pancreatic cancer cells induced by oridonin through endoplasmic reticulum stress

Objective To investigate the mechanism of oridonin inducing apoptosis of pancreatic cancer cells through endoplasmic reticulum stress.Methods Pancreatic cancer SW1990 and Panc-1 cell line were selected as the research object. Cell proliferation and apoptosis were detected by cell counting kit-8 (CCK-8) and flow cytometry respectively. The protein expression levels of endoplasmic reticulum stress-related factors glucose regulated protein 78 kD (GRP78), C/EBP-homologous protein (CHOP), cleaved cystein aspartate specific proteinase-12 (Caspase-12), active Caspase-3, cleaved Caspase-3, and cleaved poly (ADP-ribose) polymerase (PARP) were analyzed by Western blotting. The mRNA expression levels of GRP78, CHOP and Caspase-12 were detected by RT-qPCR. Results The proliferation of SW1990 and PANG-1 cells was inhibited by oridonin concentration and time correlation. The apoptosis of SW1990 and Panc-1 cells was induced and protein expression levels of cleaved caspase-3 and cleaved PARP in SW1990 cells increased by oridonin (P < 0.05). Further studies showed that oridonin up-regulated mRNA expression levels of GRP78, CHOP and Caspase-12, as well as protein expression levels of GRP78, CHOP and cleaved Caspase-12, compared with the control group, the difference was statistically significant (P < 0.05). And under the action of endoplasmic reticulum stress inhibitor 4-PBA, apoptosis rate and protein expression levels of GRP78, CHOP, cleaved Caspase-12 and active Caspase-3 were all reversed after treatment with oridonin, the difference was statistically significant (P < 0.05). Conclusion The pro-apoptotic effects of oridonin on SW1990 and Panc-1 cells are dependent on the activation of endoplasmic reticulum stress. Oridonin can mediate the apoptosis of pancreatic cancer cells by activating endoplasmic reticulum stress, which provides a new idea for the anti-tumor activity of oridonin in pancreatic cancer.