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目的:探讨胃泌素受体拮抗剂丙谷胺和特异性环氧化酶(COX)-2抑制剂NS-398对人胃腺癌细胞株MKN-45细胞凋亡的调控作用及其机制。方法:MKN-45细胞常规培养于含10%胎牛血清的RPMI1640培养液中,待细胞长至亚单层后加丙谷胺(5mmol/L)和(或)NS-398(0.01mmol/L),连续培养48h。采用流式细胞仪检测细胞凋亡率,RT-PCR法测定凋亡抑制基因bcl-2mRNA表达。结果:丙谷胺组、NS-398组和联合用药组的细胞凋亡率分别为(24.72±3.19)%、(26.69±3.35)%和(36.11±4.57)%,显著高于对照组(1.57±0.55)%(P<0.01),联合用药组的细胞凋亡率明显高于丙谷胺或NS-398单一用药组[(36.11±4.57)%vs(24.72±3.19)%和(26.69±3.35)%,P<0.05]。丙谷胺和NS-398显著下调bcl-2mRNA在MKN-45细胞的表达(P<0.05)。结论:丙谷胺、NS-398通过下调胃癌细胞bcl-2基因表达而诱导细胞凋亡,两者联合使用具有协同作用。
AIM: To investigate the regulatory effect of gastrin receptor antagonist promethazine and specific cyclooxygenase (COX) -2 inhibitor NS-398 on human gastric adenocarcinoma cell line MKN-45 and its possible mechanism. Methods: MKN-45 cells were cultured in RPMI1640 medium supplemented with 10% fetal bovine serum. When the cells grew to subunit, they were treated with 5 mmol / L and / or NS-398 (0.01 mmol / L ), Continuous training 48h. The rate of apoptosis was detected by flow cytometry, and the expression of bcl-2 mRNA was detected by RT-PCR. Results: The apoptotic rates in the valproate group, the NS-398 group and the combination group were (24.72 ± 3.19)%, (26.69 ± 3.35)% and (36.11 ± 4.57)%, respectively, which were significantly higher than those in the control group (36.11 ± 4.57)% vs (24.72 ± 3.19)% and (26.69 ± 3.35)%, respectively (P <0.01). The apoptotic rate of the combination group was significantly higher than that of the control group )%, P <0.05]. Prostamine and NS-398 significantly downregulated the expression of bcl-2 mRNA in MKN-45 cells (P <0.05). CONCLUSION: Promethazine and NS-398 induce apoptosis by down-regulating bcl-2 gene expression in gastric cancer cells.