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目的:探讨环氧合酶2(COX-2)抑制剂塞来昔布对胃癌SGC7901细胞株的放射增敏作用及其机制。方法:MTT法检测塞来昔布对胃癌SGC7901细胞株的抑制作用,计算出塞来昔布的半数抑制浓度(IC50);克隆形成实验用于检测20%IC50这个浓度的塞来昔布对胃癌SGC细胞是否具有放射敏感性;流式细胞术(FCM)分析细胞周期的分布情况。结果:MTT实验显示塞来昔布对SGC7901细胞株的抑制率随浓度的升高而升高,48 h的IC50是34.38μmol/L;克隆形成实验显示,照射组+药物组与单纯照射组相比,反映放射敏感性指标的存活分数(SF2)、平均致死剂量(D0)及准阈剂量(Dq)均下降,放射增敏比(SER)升高。FCM检测细胞周期G2和M期细胞比例增加,S期细胞比例减少。结论:塞来昔布能增加胃癌SGC7901细胞的放射敏感性,其机制可能与其抑制肿瘤细胞亚致死性损伤修复能力和促进肿瘤细胞周期再分布有关。
Objective: To investigate the radiosensitization effect of celecoxib, a cyclooxygenase 2 (COX-2) inhibitor, on gastric cancer cell line SGC7901 and its mechanism. Methods: The inhibitory effect of celecoxib on gastric cancer cell line SGC7901 was detected by MTT assay, and the half inhibitory concentration (IC50) of celecoxib was calculated. Clonogenic assay was used to detect the effect of celecoxib with 20% IC50 on gastric cancer SGC Whether the cells have radiosensitivity; Flow Cytometry (FCM) to analyze the distribution of the cell cycle. Results: The MTT assay showed that the inhibitory rate of celecoxib to SGC7901 cell line increased with the increase of concentration, and the IC50 at 48 h was 34.38 μmol / L. Clone formation assay showed that the irradiation group + drug group (SF2), mean lethal dose (D0), and quasi-threshold dose (Dq), which reflect the radiosensitivity index, decreased and the radio-sensitization ratio (SER) increased. FCM detection of cell cycle G2 and M phase increased the proportion of cells, S phase cells decreased. CONCLUSION: Celecoxib can increase the radiosensitivity of gastric cancer SGC7901 cells, and its mechanism may be related to its ability of restoring tumor cell sublethal injury repair and promoting tumor cell cycle redistribution.