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顺铂通过抑制RIP活性增强rhTRAIL杀伤肺癌A549细胞 被引量:1

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摘要 目的探讨顺铂(DDP)通过抑制受体相互作用蛋白(RIP)增强肺癌细胞A549对肿瘤坏死因子相关的凋亡诱导配体(TRAIL)敏感性的分子机制。方法 Western印迹检测顺铂、Nec-1作用A549细胞后RIP的蛋白表达。MTT法检测联合应用DDP+rh TRAIL和Nec-1+rh TRAIL作用后A549细胞的生长抑制率。Western印迹检测DDP+rh TRAIL和Nec-1+rh TRAIL对A549凋亡相关蛋白caspase-8的活化情况。流式细胞仪检测DDP+rh TRAIL和Nec-1+rh TRAIL作用后对A549细胞凋亡的影响。结果 DDP和Nec-1能显著降低A549细胞中RIP的蛋白水平,DDP、Nec-1联合rh TRAIL可以实现caspase-8的活化,促进rh TRAIL对A549细胞的杀伤作用,凋亡率从(5.9±4.93)%提高到(60.5±4.93)%和(64.1±5.17)%(P<0.01)。抑制率分别提高到(65.5±4.93)%和(76.3±9.52)%(P<0.01)。结论抑制RIP蛋白活性能增加A549细胞对rh TRAIL诱导细胞凋亡的敏感性,有利于促进rh TRAIL蛋白在治疗NSCLC方面的应用。
出处 《中国老年学杂志》 CAS CSCD 北大核心 2016年第2期276-278,共3页 Chinese Journal of Gerontology
基金 吉林省卫生厅资助项目(20082036)
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