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目的:探讨龙葵素对前列腺癌细胞Du145凋亡的分子机制。方法:应用MTT法检测龙葵素对Du145细胞活力的影响,流式细胞仪检测龙葵素对Du145细胞中活性氧的生成及细胞凋亡的影响,Western blot法检测龙葵素对细胞内p38和p-p38蛋白表达的影响。结果:10、20、40、80、160μg/ml龙葵素作用细胞24h后,细胞活力呈浓度依赖性降低。ROS抑制剂(NAC)预处理细胞1h能显著抑制龙葵素对细胞活力的抑制作用。40μg/ml龙葵素作用细胞24h能促进细胞ROS生成和细胞凋亡,细胞凋亡率为(31.0±0.8)%,与正常对照组相比具有显著统计学差异;龙葵素能促进p38磷酸化水平为(2.40±0.22)倍,与正常对照组相比具有显著统计学差异。p38磷酸化抑制剂和NAC均能显著抑制龙葵素诱导的细胞凋亡和p38的磷酸化。结论:龙葵素可诱导Du145细胞ROS的产生,通过激活p38通路诱导细胞凋亡。
Objective: To investigate the molecular mechanism of solanine on the apoptosis of prostate cancer cell line Du145. Methods: The effects of solanil on the viability of Du145 cells were detected by MTT assay. The effects of solanil on the production of reactive oxygen species (ROS) and the apoptosis of Du145 cells were detected by flow cytometry. And p-p38 protein expression. RESULTS: After treated with solanine for 10, 20, 40, 80 and 160μg / ml for 24 hours, cell viability decreased in a concentration-dependent manner. Pretreatment with ROS inhibitor (NAC) for 1 h significantly inhibited solanine on cell viability. 40μg / ml solanine could promote ROS generation and apoptosis of cells, apoptosis rate was (31.0 ± 0.8)%, which was significantly different from normal control group; solanine could promote p38 phosphorylation The level of (2.40 ± 0.22) times, compared with the normal control group had significant statistical difference. Both p38 phosphorylation inhibitor and NAC significantly inhibited solanine-induced apoptosis and phosphorylation of p38. CONCLUSION: Solanil can induce ROS production in Du145 cells and induce apoptosis by activating p38 pathway.