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作 者:张林西[1] 金春亭[1] 李玉珍[1] 李海军[1] 武欣[1] 范婕[1]
机构地区:[1]河北北方学院医学院病理学教研室,张家口075029
出 处:《肿瘤》2007年第3期181-185,共5页Tumor
基 金:河北省自然科学基金资助课题(编号:C200 5000664)
摘 要:目的:探讨COX-2抑制剂阿司匹林对食管癌细胞作用的生物学效应及可能的作用机制。方法:采用MTT法检测阿司匹林对Eca-109和TE-13细胞生长的抑制作用;FCM法检测细胞凋亡及COX-2、bcl-2,Bax基因蛋白的表达;用RIA法检测培养上清中PGE_2的含量。结果:阿司匹林可抑制2种细胞的生长,并随药物浓度升高及作用时间延长抑制率逐渐增高,而使这2株细胞产生的PGE_2量明显降低。阿司匹林还能使2株细胞的G_0/G_1期细胞显著增多,S期细胞显著减少(P<0.01),并引起了明显的细胞凋亡。2株细胞随阿司匹林作用时间的增加,COX-2和bcl-2表达显著减少,而Bax表达显著增高,COX-2、bcl-2和Bax的表达呈显著相关性(P<0.01)。结论:阿司匹林能抑制食管癌细胞的增殖并可诱导其凋亡,对食管癌进行化学预防或辅助治疗具有可能性。Objective: To investigate the biological effects of aspirin on esophageal carcinoma cells and the possible mechanism. Methods.. The inhibitory effects of aspirin on proliferation of esophageal carcinoma cell lines Eca-109 and TE-13 were measured by MTT assay. Cyclooxygenase (COX)-2, Bcl-2 and Bax protein expression and apoptosis induced by aspirin of the two cell lines were detected by flow cytometry (FCM). Progesterone E2 (PGE2) in the supernatants of cell culture was measured by radioimmunoassay (RIA). Results: Aspirin inhibited the proliferations of Eca-109 and TE-13 cells in a concentration- and time- dependent manner, but decreased the PGE2 level produced by the two cell lines. Aspirin treatment arrested the two cell lines at G0/G1 phase, reduced the proportion of S phase significantly (P〈0. 01), and induced apparent apoptosis. Aspirin time-depend- ently decreased the expressions of COX-2 and Bcl-2 and increased the expression of Bax of the two cell lines. Expressions of COX-2 and Bcl-2 had significant correlations with expression of Bax (P〈0.01). Conclusion: Aspirin inhibits the proliferation and indues apoptosis of esophageal carcinoma cells. COX-2 inhibitors has the potential to be used in the chemoprevention or adjuvant treatment for esophageal carcinomas.
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