中国肿瘤临床
中國腫瘤臨床
중국종류림상
CHINESE JOURNAL OF CLINICAL ONCOLOGY
2013年
8期
436-439
,共4页
刘斌%刘太香%白明%王伟%刘锐%邓婷%周礼鲲%巴一
劉斌%劉太香%白明%王偉%劉銳%鄧婷%週禮鯤%巴一
류빈%류태향%백명%왕위%류예%산정%주례곤%파일
芹菜素%阿司匹林%结肠癌%环氧合酶-2
芹菜素%阿司匹林%結腸癌%環氧閤酶-2
근채소%아사필림%결장암%배양합매-2
apigenin%aspirin%colorectal cancer%cyclooxygenase-2
目的:研究芹菜素(apigenin)能否增强阿司匹林(aspirin)对结肠癌细胞系的增殖抑制作用,并阐述其机制.方法:选取HT-29、HCA-7、Moser和DLD-1细胞系,设置空白对照组、芹菜素(10μmol/L)组、阿司匹林(2.5、5、10 mmol/L)组、联合用药组.MTT法检测细胞存活率.免疫印迹法和逆转录多聚酶链式反应(RT-PCR)检测不同处理方式对Moser细胞环氧合酶-2(cy?clooxygenase-2,COX-2)表达的影响.免疫印迹法检测不同处理方式对由TNF-α诱导的IκBα降解的抑制,以此来反映不同处理方式对NF-κB活性的影响.结果:芹菜素呈剂量和时间依赖性地增强阿司匹林对表达COX-2的结肠癌细胞增殖的抑制,并协同增强阿司匹林对COX-2表达的抑制和对TNF-α诱导的IκBα降解的抑制.结论:芹菜素能通过抑制COX-2的表达而增强阿司匹林对结肠癌细胞的增殖抑制.
目的:研究芹菜素(apigenin)能否增彊阿司匹林(aspirin)對結腸癌細胞繫的增殖抑製作用,併闡述其機製.方法:選取HT-29、HCA-7、Moser和DLD-1細胞繫,設置空白對照組、芹菜素(10μmol/L)組、阿司匹林(2.5、5、10 mmol/L)組、聯閤用藥組.MTT法檢測細胞存活率.免疫印跡法和逆轉錄多聚酶鏈式反應(RT-PCR)檢測不同處理方式對Moser細胞環氧閤酶-2(cy?clooxygenase-2,COX-2)錶達的影響.免疫印跡法檢測不同處理方式對由TNF-α誘導的IκBα降解的抑製,以此來反映不同處理方式對NF-κB活性的影響.結果:芹菜素呈劑量和時間依賴性地增彊阿司匹林對錶達COX-2的結腸癌細胞增殖的抑製,併協同增彊阿司匹林對COX-2錶達的抑製和對TNF-α誘導的IκBα降解的抑製.結論:芹菜素能通過抑製COX-2的錶達而增彊阿司匹林對結腸癌細胞的增殖抑製.
목적:연구근채소(apigenin)능부증강아사필림(aspirin)대결장암세포계적증식억제작용,병천술기궤제.방법:선취HT-29、HCA-7、Moser화DLD-1세포계,설치공백대조조、근채소(10μmol/L)조、아사필림(2.5、5、10 mmol/L)조、연합용약조.MTT법검측세포존활솔.면역인적법화역전록다취매련식반응(RT-PCR)검측불동처리방식대Moser세포배양합매-2(cy?clooxygenase-2,COX-2)표체적영향.면역인적법검측불동처리방식대유TNF-α유도적IκBα강해적억제,이차래반영불동처리방식대NF-κB활성적영향.결과:근채소정제량화시간의뢰성지증강아사필림대표체COX-2적결장암세포증식적억제,병협동증강아사필림대COX-2표체적억제화대TNF-α유도적IκBα강해적억제.결론:근채소능통과억제COX-2적표체이증강아사필림대결장암세포적증식억제.
Objective:This study aimed to determine whether apigenin can enhance the inhibitory effect of aspirin on colorectal cancer cell lines and to investigate the underlying mechanism in vitro. Methods:The colorectal cancer cell lines HT-29, HCA-7, Moser, and DLD-1 were selected for this study. All cell lines were divided into four groups:control group, group treated with 10μmol/L api-genin, group treated with aspirin at 2.5, 5, and 10 mmol/L, and group treated with apigenin and aspirin at varying concentrations. Api-genin was applied 2 h prior to aspirin addition. Cell viability was detected by MTT assay at 24, 48, and 72 h post-treatment. Western blot and reverse-transcription polymerase chain reaction analysis were performed to determine the effect of different treatments on the expression of COX-2 in Moser cells 48 h after treatment. Protection of IκBαdegradation by TNF-αtreatment was detected by Western blot analysis to validate the effect of apigenin and aspirin against NF-κB activation. Results:Apigenin enhanced the inhibitory effect of aspirin on colorectal cancer cells in a dose-and time-dependent manner. The effect was correlated with the suppression of COX-2 ex-pression. COX-2 expression was markedly inhibited in the combined treatment group. In addition, combined treatment resulted in a re-markable inhibition of the TNF-α-induced degradation of IκBα. Conclusion:Apigenin can potentiate the inhibitory effect of aspirin on colorectal cancer cells by inhibiting COX-2 expression.