摘要
目的探讨泮托拉唑对胃癌细胞MKN-45增殖与凋亡的影响及相关机制。方法采用0、10、20、40μg/ml的泮托拉唑处理MKN-45细胞48 h;MTT法检测细胞活力;Hoechst染色检测细胞形态;流式细胞术检测细胞周期;Western blot检测细胞中B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、细胞周期蛋白D1(Cyclin D1)及Cyclin E表达。结果与0μg/ml比较,10、20、40μg/ml的泮托拉唑能明显降低MKN-45细胞活力(P﹤0.01),使细胞核发白,皱染,使细胞周期阻滞在G1期(P﹤0.01),下调Cyclin D1及Cyclin E的表达(P﹤0.01);与0μg/ml比较,20、40μg/ml的泮托拉唑能明显下调MKN-45细胞中Bcl-2的表达(P﹤0.01),上调Bax的表达(P﹤0.01)。结论泮托拉唑通过调控细胞周期蛋白及细胞凋亡相关蛋白表达抑制胃癌细胞MKN-45的增殖,并诱导细胞凋亡。
Objective To explore the effect of pantoprazole on the proliferation and apoptosis in gastric cancer cell MKN-45 and the underlying mechanism. Method MKN-45 cell was treated with 0, 10, 20, and 40 μg/ml pantoprazole for 48 h; cell viability was measured by MTT assay; cell morphology was detected by Hoechst staining; cell cycle was determined by flow cytometry; the expression of B-cell lymphoma-2（Bcl-2）, Bcl-2 associated X protein（Bax）, Cyclin D1 and Cyclin E were measured by western blot. Result Compared with 0 μg/ml, treatment of 10, 20, 40 μg/ml pantoprazole reduced cell viability（P〈0.01）, resulting in dense and thick white cell nucleus, with cell cycle arrested in G1 phase（P〈0.01）, besides, the expression of Cyclin D1 and Cyclin E was down-regulated（P〈0.01）. 20 and 40 μg/ml pantoprazole might markedly down regulate the expression of Bcl-2（P〈0.01）, while up regulate the expression of Bax（P〈0.01）. Con Conclusion Pantoprazole could inhibit MKN-45 cell proliferation and induce cell apoptosis, by regulating expression of cell cyclin and apoptosis related protein.
出处
《癌症进展》
2018年第2期171-174,共4页
Oncology Progress
关键词
泮托拉唑
胃癌细胞
MKN-45
增殖
凋亡
pantoprazole
gastric cancer cell
MKN-45
proliferation
apoptosis
