全反式维甲酸联合阿司匹林对体外抑制肺腺癌细胞株A549增殖和促凋亡的作用及其机制

发布时间：2018-03-10 09:06

本文选题：全反式维甲酸　切入点：阿司匹林　出处：《中国医院药学杂志》2017年20期 　论文类型：期刊论文

【摘要】：目的:观察全反式维甲酸(ATRA)联合阿司匹林(ASA)体外抑制肺癌A549细胞增殖,促凋亡作用和机制。方法:体外培养人肺腺癌A549细胞,5,10μmol·L-1的ATRA单独及分别联合5,10μmol·L-1的ASA进行干预48 h、72 h后,MTT法检测细胞增殖抑制率;TUNEL法观测药物作用48 h后细胞凋亡状态;RT-PCR法检测药物作用后肺腺癌A549细胞COX-2 mRNA的表达;Western blot法检测凋亡相关因子Bax、Bcl-2、COX-2和caspase-3蛋白的表达。结果:ATRA与ASA联用对A549增殖具有协同作用;TUNEL法结果显示ATRA可诱导A549细胞凋亡,与ASA联用凋亡率显著升高(P0.05);RT-PCR显示A579细胞中COX-2 mRNA呈现高表达状态,ASA可下调COX-2表达,ATRA无此作用;Western blot结果显示ATRA和ASA协同作用使A549细胞中Bcl-2、COX-2蛋白表达受到抑制,Bax蛋白表达增加,Bcl-2/Bax值降低,对凋亡通路的影响大于单药作用(P0.05)。结论:ASA联合ATRA可协同抑制肺腺癌细胞A549的增殖及以及促进其发生凋亡,其作用机制可能是ASA通过抑制COX-2蛋白表达,与ATRA共同通过Bcl/caspase通路诱导肿瘤凋亡实现的。
[Abstract]:Objective: to observe the inhibitory effect of ATRAA combined with aspirin on proliferation of lung cancer A549 cells in vitro. Methods: human lung adenocarcinoma A549 cells were cultured in vitro with 10 渭 mol 路L -1 ATRA and 5 10 渭 mol 路L -1 ASA for 48 h and 72 h later, the inhibition rate of cell proliferation was measured by Tunel method and apoptosis was measured by Tunel method. The expression of COX-2 mRNA in lung adenocarcinoma A549 cell line was detected by RT-PCR and the expression of apoptosis related factor BaxanBcl-2 COX-2 and caspase-3 protein was detected by Western blot. Results the results showed that ATRA could induce apoptosis of A549 cells by TUNEL-mediated dUTP Nick end labeling (Tunel). The expression of COX-2 mRNA in A579 cells was significantly increased by RT-PCR combined with ASA. The results showed that the expression of COX-2 mRNA in A579 cells was down-regulated. The results showed that ATRA and ASA combined with ASA could inhibit the expression of Bcl-2COX-2 protein in A549 cells and inhibit the expression of Bcl-2COX-2 protein in A549 cells. The results showed that the expression of Bcl-2COX-2 protein in A549 cells was inhibited by the synergistic effect of ATRA and ASA. The value of Bcl-2 / Bax decreased, Conclusion ATRA combined with ATRA can synergistically inhibit the proliferation and induce apoptosis of lung adenocarcinoma cell line A549, and its mechanism may be that ASA inhibits the expression of COX-2 protein. In combination with ATRA, apoptosis was induced by Bcl/caspase pathway.
【作者单位】：武汉市第四医院心胸外科;
【分类号】：R734.2

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