目的体外观察塞来昔布对大肠癌细胞株HT-29细胞增殖和凋亡的影响,探讨其可能的作用机制。方法采用噻唑蓝(MTT)比色法,流式细胞(FCM)、吖啶橙/溴化乙啶染色结合荧光显微镜、Western印迹法等技术,研究塞来昔布对HT-29细胞增殖的抑制和可能的机制。结果塞来昔布抑制HT-29细胞生长,呈浓度和时间依赖性。流式术检测出典型的亚二倍体“凋亡峰”,凋亡率(7.31±2.37)%~(48.30±2.86)%;使G0/G1期细胞比例升高,S期和G2/M期比例缩小、细胞核固缩、凋亡小体形成等。凋亡比例呈剂量和时间依赖。塞来昔布降低细胞周期素依赖蛋白激酶CDK2和CDK4的表达、上调细胞周期素依赖蛋白激酶抑制因子P21WAF1/CIP1n蛋白表达。结论体外塞来昔布抑制HT-29细胞增殖,并诱导细胞凋亡;下调CDK_2和CDK_4蛋白表达,上调P21WAF1/CIP1n蛋白表达。塞来昔布抑制HT-29细胞增殖、诱导凋亡可能与阻止细胞周期进展有关。 Objective To observe the effect of celecoxib on the proliferation and apoptosis of colorectal cancer cell line HT-29 in vitro and to explore its possible mechanism. Methods MTT assay, flow cytometry (FCM), acridine orange / ethidium bromide staining combined with fluorescence microscopy and Western blotting were used to study the inhibitory effect of celecoxib on the proliferation of HT-29 cells And possible mechanisms. Results Celecoxib inhibited HT-29 cell growth in a concentration and time-dependent manner. Flow cytometry showed typical sub-diploid “apoptotic peak” with a apoptotic rate of (7.31 ± 2.37)% ~ (48.30 ± 2.86)%. The proportion of cells in G0 / Phase reduction, nuclear condensation, apoptotic body formation and so on. Apoptosis was dose-and time-dependent. Celecoxib decreased the expression of cyclin-dependent protein kinases CDK2 and CDK4 and upregulated the expression of cyclin-dependent protein kinase inhibitor P21WAF1 / CIP1n. CONCLUSION: Celecoxib inhibits the proliferation and induces apoptosis of HT-29 cells in vitro, down-regulates the expressions of CDK_2 and CDK_4, and up-regulates the expression of P21WAF1 / CIP1n. Celecoxib inhibited the proliferation of HT-29 cells and induced apoptosis may be related to the prevention of cell cycle progression.