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作 者:李安飞[1] 罗海丹[1] 陈昱 苏箔金 王冬辉[1] 杨惠玲[1]
机构地区:[1]中山大学中山医学院病理生理教研室,广东广州510080
出 处:《中国病理生理杂志》2017年第11期1980-1986,共7页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.81372410);广东省科技计划(No.2013B031800002;No.2015A020211006)
摘 要:目的:探讨阿司匹林诱导同源不同辐射抗拒能力鼻咽癌细胞株CNE2R/CNE2凋亡的作用及其机制。方法:采用MTT法、流式细胞术和Western blot法检测并比较阿司匹林对CNE2R和CNE2细胞活力、细胞凋亡及凋亡相关蛋白procaspase-3、cleaved caspase-3、procaspase-9、procaspase-12、PARP、cleaved PARP、Bcl-2和Bax,以及PI3K p110α、Akt和p27蛋白水平的影响。结果:阿司匹林抑制同源不同辐射抗拒能力细胞CNE2R/CNE2的活力(阿司匹林对CNE2细胞作用24、48和72 h的IC50分别为6.18、3.92和3.06 mmol/L,对CNE2R细胞作用24、48和72 h的IC50分别为7.05、3.90和2.20 mmol/L,两者差异无统计学显著性)。阿司匹林作用48 h后,CNE2R细胞凋亡率升高,明显高于CNE2细胞(P<0.05)。阿司匹林作用48 h后,CNE2和CNE2R细胞中procaspase-3、procaspase-9、procaspase-12和PARP的蛋白水平降低,cleaved caspase-3和cleaved PARP的蛋白水平升高(P<0.05);PI3K p110α和Akt蛋白水平下降,Bcl-2水平降低,Bax水平升高,Bcl-2/Bax比值降低,p27水平升高(P<0.05)。结论:阿司匹林对同源不同辐射抗拒能力鼻咽癌细胞株CNE2R和CNE2具有同等细胞活力抑制作用;并且可以诱导细胞凋亡,且对抗辐射细胞株CNE2R的凋亡诱导作用更明显。阿司匹林的抗癌作用可能与其影响PI3K/Akt信号通路及其下游蛋白的水平有关。AIM:To investigate the effects of aspirin on the apoptosis of nasopharyngeal carcinoma cell lines CNE2 R and CNE2 with different radioresistance and its potential mechanism.METHODS:The effects of aspirin on the cell viability,apoptosis,and protein levels of procaspase-3,cleaved caspase-3,procaspase-9,procaspase-12,PARP and cleaved PARP,PI3 K p110α,Akt,Bcl-2,Bax and p27 in the CNE2 R cells and CNE2 cells were detected by the methods of MTT assay,flow cytometry and Western blot.RESULTS:Aspirin inhibited the viability of homologous nasopharyngeal carcinoma cell lines CNE2 and CNE2 R(with the IC50 to CNE2 cells of 6.18,3.92 and 3.06 mmol/L for 24 h,48 h and72 h,respectively;and with the IC50 to CNE2 R cells of 7.05,3.90 and 2.20 mmol/L for 24 h,48 h and 72 h,respectively).After treated with aspirin for 48 h,the apoptotic rate of CNE2 R cells was higher than that of CNE2 cells(P 〈0.05).After treated with aspirin for 48 h,the protein levels of procaspase-3,procaspase-9,procaspase-12 and PARP were decreased,the protein levels of cleaved caspase-3,cleaved PARP and p27 were increased,and the protein levels of PI3 K p110α,Akt and Bcl-2/Bax were decreased.CONCLUSION:Aspirin inhibits the viability of homologous nasopharyngeal carcinoma cell lines CNE2 R and CNE2 with different radioresistance.Aspirin also induces the apoptosis of CNE2 and CNE2 R cells,which is more effective in CNE2 R cells.The underlying mechanisms may be involved in affecting PI3 K/Akt signaling pathway,Bcl-2/Bax and p27 expression.
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