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目的 探讨奥美拉唑致胃上皮凋亡及其作用机制。方法 采用流式细胞仪 ,测定奥美拉唑对SGC 790 1细胞株细胞周期、细胞凋亡发生的影响 ,并检测 p5 3、GADD4 5、p15 ,16 ,18,19和bcl 2的表达改变和ATP合酶活性。同时用TUNEL法检测奥美拉唑作用原代胃上皮细胞的凋亡情况。结果 奥美拉唑作用 2 4h引起SGC 790 1细胞周期发生显著改变 ,G1期百分比减少 ,G2 期百分比增加 ,以后者改变较明显 ,然无细胞凋亡峰出现 ,作用 72h出现细胞凋亡峰。p5 3、GADD4 5、p15 ,16 ,18,19和bcl 2表达均无显著改变 ,奥美拉唑作用前胞内ATP合酶活性为 0 .32 6～ 0 .387,奥美拉唑作用 72h后显著下降为 0 .0 5 4～ 0 .10 3。奥美拉唑致胃黏膜细胞凋亡发生率显著高于对照组 (P <0 .0 1)。结论 奥美拉唑通过线粒体途径导致胃上皮细胞凋亡 ,对治疗更新速率较快的伴DNA氧化性损伤胃上皮有重要意义
Aim To investigate the apoptosis of gastric epithelium induced by omeprazole and its mechanism. Methods The effects of omeprazole on the cell cycle and apoptosis of SGC 7901 cell line were determined by flow cytometry. The expression of p5 3, GADD4 5, p15, 16, 18, 19 and bcl 2 ATP synthase activity. At the same time, the apoptosis of primary gastric epithelial cells treated with omeprazole was detected by TUNEL method. Results Omeprazole caused a significant change in the cell cycle of SGC 7901 cells after 24 h treatment. The percentage of cells in G1 phase decreased and the percentage of G2 phase increased. The latter changed more obviously, but no apoptotic peak appeared. p5 3, GADD4 5, p15, 16, 18, 19 and bcl 2 had no significant change, the activity of intracellular ATP synthase before omeprazole was 0.326 ~ 0.387, omeprazole 72h After the significant decline to 0. 0 5 4 ~ 0. 10 3. The incidence of gastric mucosal apoptosis in omeprazole group was significantly higher than that in control group (P <0.01). Conclusion Omeprazole causes apoptosis of gastric epithelial cells through the mitochondrial pathway, which is of great significance for the treatment of oxidative damage to the gastric epithelium with a higher update rate