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目的 :研究非甾体类抗炎药吲哚美辛诱导人胃癌细胞系SGC 790 1的凋亡作用及对COX 2mRNA表达及c myc、bcl 2、cas pase 3凋亡基因蛋白的表达 ,以探索其凋亡机制。方法 :胃癌细胞的凋亡用电子显微镜、AnnexinV FITC染色流式细胞仪技术测定。COX 2基因表达用RT PCR法测定。c myc、bcl 2和caspase 3蛋白表达用免疫细胞化学技术测定。结果 :吲哚美辛在浓度为 50 μmol/L时作用48、72h和浓度为 1 0 0和 2 0 0 μmol/L时作用 2 4、48、72h均可诱导胃癌细胞凋亡 ,凋亡率分别为 6 .48%、8.2 0 % ;9.1 4 %、1 2 .2 7%、1 5 .1 1 %和 9.95 %、1 4 .70 %、1 9.81 % ,呈浓度和时间依赖性。吲哚美辛可降低COX 2mRNA表达和bcl 2蛋白表达 ,增加c myc和caspase 3蛋白表达。 2 0 0 μmol/L吲哚美辛作用 72h ,bcl 2、c myc和caspase 3蛋白表达阳性率分别为 2 2 .8± 6 .5 %、42 .5± 1 3 .1 %和 31 8± 1 2 .7% ;对照组为 44 .6± 1 0 .1 %、2 4 .74± 9.5 %和 1 4 .8± 6 .4%。两者比较 ,差异有显著性 (P <0 .0 1 )。结论 :吲哚美辛可诱导胃癌细胞SGC 790 1凋亡 ,其机制涉及bcl 2表达下调、c myc表达上调及caspase 3激活。说明多基因调控参与其中
AIM: To investigate the apoptosis of human gastric cancer cell line SGC-7901, a non-steroidal anti-inflammatory drug induced by indomethacin, and the expression of COX-2 mRNA and c-myc, bcl-2 and caspase- Its mechanism of apoptosis. Methods: The apoptosis of gastric cancer cells was determined by electron microscopy and Annexin V FITC staining. COX 2 gene expression was measured by RT PCR. The expressions of c-myc, bcl-2 and caspase-3 proteins were determined by immunocytochemistry. Results: Indomethacin could induce gastric cancer cell apoptosis at a concentration of 50 μmol / L for 48 and 72 h and at a concentration of 100 and 200 μmol / L for 2, 48, and 72 h Respectively, which were 6.48%, 8.2%, 9.14%, 12.27%, 15.1% and 9.95%, 14.7% and 1 9.81%, respectively, in a concentration- and time-dependent manner. Indomethacin decreases COX 2 mRNA expression and bcl 2 protein expression, and increases c-myc and caspase 3 protein expression. The positive rates of bcl-2, c-myc and caspase-3 protein after 72 hours exposure to indometacin at 200 μmol / L were 42.8 ± 6.5%, 42.5 ± 13.1% and 31.8 ± 12.7% in the control group, 44.6 ± 10.1%, 24.79 ± 9.5% and 14.8 ± 6.4% in the control group. The difference between the two groups was significant (P <0.01). Conclusion: Indomethacin can induce the apoptosis of SGC-7901 gastric cancer cells. Its mechanism involves the down-regulation of bcl-2, up-regulation of c-myc and activation of caspase-3. Multi-gene regulation that involved