丙泊酚在低氧条件下对胰腺癌细胞增殖和侵袭的影响及可能的机制

Effect of propofol on the proliferation and invasion of pancreatic cancer cells under hypoxic conditions and the underlying mechanism

目的 探讨丙泊酚在低氧条件下对胰腺癌细胞增殖和侵袭的影响及其可能的机制。方法 胰腺癌Panc-1细胞株在常规条件下培养24 h后,将细胞随机分为Hypo组(低氧)、Hypo+P组(低氧+10μg/ml丙泊酚培养)和正常组(正常培养)。其中Hypo组和Hypo+P组在低氧培养箱中继续培养,正常组在常规条件下继续培养。采用CCK8法检测细胞增殖能力,Transwell实验检测细胞侵袭能力,蛋白质印迹法检测解整合素样金属蛋白酶8(ADAM8)蛋白表达情况。结果 培养24、48、72 h,Hypo组胰腺癌Panc-1细胞的增殖活性均高于正常组和Hypo+P组,差异均有统计学意义(P﹤0.05)。Hypo组胰腺癌Panc-1细胞侵袭数目多于正常组和Hypo+P组,ADAM8蛋白相对表达量高于正常组和Hypo+P组,差异均有统计学意义(P﹤0.05)。结论 丙泊酚在低氧条件下对胰腺癌细胞的增殖和侵袭具有抑制作用,其机制可能与抑制ADAM8蛋白表达有关。

Objective To investigate the effect of propofol on the proliferation and invasion of pancreatic cancer cells under hypoxic conditions and its underlying mechanism. Method Pancreatic cancer Panc-1 cell was cultured under conventional conditions for 24 h, and the cells were randomly divided into Hypo group(hypoxia), Hypo+P group(hypoxia+10 μg/ml propofol), and normal group(normal culture). Among them, the Hypo group and the Hypo+P group were continued to be cultured in a hypoxic incubator, and the normal group was continued to be cultured under conventional conditions. Cell proliferation was detected by CCK8 assay. Cell invasion was detected by Transwell assay. The protein expression of a disintegrin and metalloproteinase domain 8(ADAM8) was detected by Western blot. Result After 24, 48, and 72 h of culture, the proliferation activity of Panc-1 cells in the Hypo group were higher than those in the normal group and the Hypo+P group, and the differences were statistically significant(P<0.05). The number of Panc-1 cells invaded in the Hypo group was more than that in the normal group and the Hypo+P group, and the relative expression of ADAM8 protein was higher than that in the normal group and the Hypo+P group, and the differences were statistically significant(P<0.05). Conclusion Propofol has inhibitory effects on the proliferation and invasion of pancreatic cancer cells under hypoxic conditions, and its underlying mechanism may be related to the inhibition of ADAM8 expression.