论文部分内容阅读
目的:探讨ERK信号传导通路在β-榄香烯诱导肾癌细胞凋亡中的作用。方法:以人肾透明细胞癌786-0细胞为研究对象,四甲基偶氮唑蓝(MTT)比色法测定细胞活力;流式细胞术碘化丙啶(PI)染色检测细胞凋亡;蛋白印迹法检测细胞内磷酸化ERK及总ERK的表达水平。为研究ERK通路活性对β-榄香烯抗肿瘤作用的影响,将实验分为空白对照组,β-榄香烯单药组(160μg/mL)、ERK抑制剂组(PD98059,20μmol/L)和联合用药组(PD98059+β-榄香烯)。结果:40、80、160及320μg/mL的β-榄香烯作用于786-0细胞24h,细胞生存率逐渐下降,分别为(83.20±4.63)%、(74.29±3.50)%、(49.75±3.08)%和(16.99±4.73)%,相邻浓度间P均<0.05。随着浓度的增加,细胞凋亡率逐渐增加。进一步研究发现,β-榄香烯可明显抑制细胞内磷酸化ERK的水平。同β-榄香烯单药组相比,联合用药组的细胞活力明显降低,差异有统计学意义〔(52.73±6.36)%vs(39.24±3.24)%〕,P<0.05。结论:β-榄香烯可能通过抑制ERK通路活性发挥对肾癌细胞的抗肿瘤作用。
AIM: To investigate the role of ERK signaling pathway in β-elemene-induced apoptosis of renal cell carcinoma. Methods: Human renal clear cell carcinoma 786-0 cells were treated with MTT assay. Cell viability was detected by flow cytometry with propidium iodide (PI) staining. The levels of phosphorylated ERK and total ERK in cells were detected by Western blotting. To study the effect of ERK pathway on the antitumor effect of β-elemene, the experiment was divided into blank control group, β-elemene single group (160μg / mL), ERK inhibitor group (PD98059, 20μmol / And combination group (PD98059 + β-elemene). Results: The cell survival rates of 786-0 cells treated with 40, 80, 160 and 320 μg / mL β-elemene decreased gradually (83.20 ± 4.63%, 74.29 ± 3.50%, 49.75 ± 3.08)% and (16.99 ± 4.73)%, P <0.05 between adjacent concentrations. With the increase of concentration, the rate of apoptosis gradually increased. Further study found that β-elemene significantly inhibited intracellular phosphorylation of ERK levels. Compared with β-elemene alone, the cell viability of the combination group was significantly lower (P <0.05). Conclusion: β-elemene may exert anti-tumor effects on renal cancer cells by inhibiting ERK pathway activity.