龙葵素通过ROS/p38信号通路诱导人前列腺癌细胞凋亡

Solanine induces the apoptosis of human prostate cancer cells via ROS/p38 signaling pathway

目的探讨龙葵素对前列腺癌细胞Du145和LNCaP凋亡的分子机制。方法应用MTT法检测龙葵素对Du145和LNCaP细胞活力的影响,流式细胞术检测龙葵素对Du145和LNCaP细胞中活性氧的生成及细胞凋亡的影响,Western印迹法检测龙葵素对细胞内p38和p-p38蛋白水平的影响。结果龙葵素能显著抑制Du145和LNCaP细胞的细胞活力,且呈现剂量依赖性(P<0.01),ROS清除剂NAC能显著抑制龙葵素对细胞活力的抑制作用。40μmol/L龙葵素作用细胞24h能诱导细胞ROS生成和细胞凋亡,并促进p38磷酸化,NAC能显著抑制龙葵素诱导的细胞凋亡和p38的磷酸化,p38磷酸化抑制剂能够显著抑制龙葵素诱导的细胞凋亡。结论龙葵素诱导ROS的产生,通过激活p38通路诱导人前列腺癌细胞凋亡。

Objective To investigate the molecular mechanism of solanine-induced apoptosis of prostate cancer cells Du145 and LNCaP.Methods The effects of solanine on the viability of Du145 and LNCaP cells were evaluated by MTT assay.The generation of intracellular reactive oxygen species(ROS)and solanine-induced apoptosis were measured by flow cytometry.The protein levels of p38 and p-p38 expressions were examined by Western blot.Results Solanine significantly inhibited the viability of Du145 and LNCaP cells in a dose-dependent manner(P<0.01).The inhibition of solanine on cell viability was suppressed by the ROS scavenger NAC.ROS generation,apoptosis and phosphorylation of p38 were induced by treatment with solanine at 40μmol/L for 24 h.The expression of p38 and solanine-induced apoptosis were suppressed by NAC and SB203580.ConclusionSolanine induces the apoptosis of human prostate cancer cell via the ROS-p38 signaling pathway.