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目的:研究新藤黄酸(Gambogenic acid,GNA)对人胃癌MGC-803细胞凋亡的影响,并探讨其抗肿瘤的作用机制。方法:MTT法检测细胞存活率;Annexin V-FITC/PI染色流式细胞术(FCM)检测MGC-803细胞凋亡率;H2DCFDA探针法流式细胞术检测细胞内活性氧的含量;罗丹明123染色FCM检测细胞线粒体膜电位(△Ψm)的改变;Western blot法检测细胞内P53蛋白的表达变化。结果:新藤黄酸在1.0~12.0μmol/L浓度范围内可抑制人胃癌细胞MGC-803细胞的增殖;增加细胞内活性氧的含量;降低线粒体膜电位;诱导细胞发生凋亡并呈浓度依赖性;Western blotting结果显示,新藤黄酸明显升高MGC-803细胞凋亡诱导基因P53的表达。结论:新藤黄酸可诱导人胃癌MGC-803细胞的凋亡,其机制可能与促进P53介导的线粒体途径依赖的细胞凋亡相关。
Objective: To study the effect of Gambogenic acid (GNA) on the apoptosis of human gastric cancer cell line MGC-803 and to explore its anti-tumor mechanism. Methods: The cell viability was detected by MTT assay; the apoptosis rate of MGC-803 cells was detected by Annexin V-FITC / PI staining; the content of reactive oxygen species (ROS) was detected by flow cytometry with H2DCFDA probe; 123 staining FCM to detect mitochondrial membrane potential (△ Ψm) changes; Western blot assay P53 protein expression changes. Results: In the range of 1.0 ~ 12.0μmol / L, the new Gambogic acid could inhibit the proliferation of human gastric cancer cell line MGC-803, increase the content of intracellular reactive oxygen species, decrease the mitochondrial membrane potential and induce cell apoptosis in a concentration-dependent manner The results of Western blotting showed that Gambogic acid significantly increased the expression of apoptosis-inducing gene P53 in MGC-803 cells. Conclusion: Gambogic acid can induce the apoptosis of human gastric cancer cell line MGC-803, which may be related to the promotion of mitochondrial pathway-dependent apoptosis mediated by P53.