龙葵素通过ROS激活p38信号通路诱导人前列腺癌Du145细胞凋亡

Solanine induces human prostate cancer Du145 apoptosis via the ROS-p38 signaling pathway

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-induced apoptosis in prostate cancer cells Du145. Methods： The influence on the viabihty of Du145 cells were evaluated by MTT assay. Intracellular reactive oxygen species （ ROS ） generation and apoptosis induced by solanine were measured by flow cytometry analysis. The protein levels of p38 and p-p38 were examined by Western blot analysis. Results： 10, 20, 40, 80, 160 μg/ml Solanine could significantly inhibited the viability of Du145 in a dose-dependent manner. The inhibition of solanine on cell viability was. suppressed by the ROS scavenger NAC. The ROS generation, apoptosis and phosphorylation of p38 was induced by treating with solanine at 40 μg/ml for 24 h. The apoptosis rate was （31.0 ± 0.8） %. The phosphorylation level of p38 increased （2.40±0.22） times. The expression of p38 and apoptosis induced by solanine were suppressed by NAC and SB203580. Conclusion： Sola- nine induces human prostate cancer Du145 cell apoptosis via the ROS-p38 signaling pathway.