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目的探讨舒林酸诱导入胃癌BGC-823细胞株凋亡的作用及其机制。方法将舒林酸作用于人胃癌BGC-823细胞,并设置不同的作用浓度和作用时间。应用流式细胞术、TUNEL法检测胃癌细胞的凋亡率;免疫组化(S-P)法检测凋亡基因蛋白bd-2、sur- vivin的表达以及环氧合酶-2(COX-2)蛋白的表达情况。结果流式细胞仪检测出凋亡峰;其凋亡检测率及TUNEL法检测的细胞凋亡率均高于对照组(P<0．05);免疫组化结果显示凋亡基因蛋白bcl-2、survivin等在胃癌细胞表达下降,COX-2蛋白的表达阳性率也显著低于对照组,均呈时间和剂量依赖性(P<0．05)。结论舒林酸可诱导胃癌BGC-823细胞凋亡,其机制与抑制凋亡抑制基因bel-2和 survivin的表达及下调COX-2蛋白的表达有关。
Objective To investigate the effect of sulindac on the apoptosis of gastric cancer cell line BGC-823 and its mechanism. Methods Sulindac was applied to human gastric cancer cell line BGC-823, and different concentration and duration of action were set. The apoptosis rate of gastric cancer cells was detected by flow cytometry and TUNEL method. The expression of bcl-2, sur-vivin and COX-2 protein were detected by immunohistochemistry (SP) The expression of the situation. Results The apoptotic peak was detected by flow cytometry. The apoptosis rate of the cells was higher than that of the control group (P <0.05). The results of immunohistochemistry showed that the apoptosis gene protein bcl-2 , Survivin in gastric cancer cells decreased, the expression of COX-2 protein was also significantly lower than the control group, both in a time and dose-dependent manner (P <0.05). Conclusion Sulindac can induce the apoptosis of gastric cancer cell line BGC-823, and its mechanism is related to inhibiting the expression of apoptosis-suppressing genes bel-2 and survivin and down-regulating the expression of COX-2 protein.