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龙葵素通过ROS/p38信号通路诱导人前列腺癌细胞凋亡
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Journal Article
龙葵素通过ROS/p38信号通路诱导人前列腺癌细胞凋亡
2017
Overview
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。
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