鱼藤素诱导人胃癌SGC7901/VCR细胞程序性坏死的作用研究
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R735.2

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广东省佛山市顺德区陈立加脾胃病专家工作室资助项目


Deguelin Can Induce Programmed Necrosis of Human Gastric Carcinoma SGC7901/VCR Cells
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    摘要:

    目的:研究鱼藤素诱导人胃癌SGC7901/VCR细胞程序性坏死的作用。方法:应用Hoechst33342/碘化丙锭(PI)染色荧光显微镜、Annexin V-FITC/PI流式细胞仪检测鱼藤素作用前后人胃癌SGC7901/VCR细胞凋亡与坏死的变化;应用透射电镜观察鱼藤素作用前后人胃癌SGC7901/VCR细胞超微结构的变化;用Western blot检测RIP1和RIP3蛋白表达情况。结果:与对照组比较,鱼藤素组可见大量坏死细胞,细胞凋亡率无明显差异,但坏死率显著升高(P<0.05);透射电镜检测发现,鱼藤素组细胞可见细胞核肿胀外突,染色质凝聚成块,核膜周边聚集形成大量坏死小体;Western blot检测结果显示,鱼藤素组细胞RIP1和RIP3蛋白表达显著升高,且随时间延长逐渐增加。结论:鱼藤素作用于人胃癌SGC7901/VCR细胞后,诱导其出现细胞程序性坏死,其机制有待进一步研究。

    Abstract:

    Objective: To observe the effect of deguelin inducing programmed necrosis of human gastric carcinoma SGC7901/VCR cells.Methods:Detected the changes of apoptosis and necrosis of human gastric carcinoma SGC7901/VCR cells before and after the induction of deguelin via Hoechst 33342/propidium iodide(PI)staining fluorescence microscope and Annexin V-FITC/PI flow cytometer;observed the changes of the ultrastructure of human gastric carcinoma SGC7901/VCR cells before and after the induction of deguelin via transmission electron microscope;detected the expression of RIP1 and RIP3 protein via Western blot.Results:Comparing with the control group,there were numerous dead cells being found in the deguelin group,and there was no significant difference being found in the apoptosis rate,while the necrosis rate was significantly increased(P< 0.05).Detected by transmission electron microscope,nuclear swelling and evagination,chromatin condensation and numerous necrosomes forming around the nuclear membrane were observed in the deguelin group.As the results of West blot showed,the expression of RIP1 and RIP3 protein of cells in the deguelin group was significantly elevated,and was gradually increased as time extended.Conclusion:After acting on human gastric carcinoma SGC7901/VCR cells,deguelin can induce their programmed necrosis,and its mechanism needs to be further studied.

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陈立加,高卓维,林清,张双喜.鱼藤素诱导人胃癌SGC7901/VCR细胞程序性坏死的作用研究[J].新中医,2018,50(6):6-9

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  • 在线发布日期: 2018-06-05
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