【作者】 吴建新；

【导师】 罗学来；

【作者基本信息】 华中科技大学 ， 外科学， 2017， 硕士

【摘要】 【目的】研究造血细胞特异性蛋白相关蛋白Hax-1(Hematopoietic cell-specific protein1-associated protein X-1)对内质网应激诱导的细胞凋亡影响。【方法】1、首先用衣霉素处理细胞,在体外成功建立细胞内质网应激(Endoplasmic Reticulum stress,ER stress)的模型,并观察细胞的凋亡和Hax-1的变化情况。2、构建可以在细胞内表达的Hax-1重组质粒。3、重组质粒转染进入细胞后,再用衣霉素处理细胞,建立内质网应激模型,研究Hax-1对内质网应激诱导的凋亡影响。【结果】1、在衣霉素诱导的内质网应激中,细胞凋亡蛋白水平升高,Hax-1表达水平明显下降。2、高表达Hax-1可抑制内质网应激诱导的细胞凋亡,减少凋亡蛋白表达。3、高表达Hax-1可以稳定线粒体膜电位,进而抑制细胞凋亡。【结论】高表达Hax-1可以抑制内质网应激诱导的细胞凋亡。更多还原

【Abstract】 ObjectivesTo investigate the effect of Hax-1 on apoptosis of cells induced by Endoplasmic Reticulum stress(ER stress).Methods1.The Endoplasmic Reticulum stress model in cells was induced by Tunicamycin in vitro,and the apoptosis of cells and expression of Hax-1 were detected.2.A recombinant plasmid of human Hax-1 was constructed,and its high expression in cells was confirmed.3.Cells were treated with Tunicamycin after the transfection of Hax-1,and the role of Hax-1 in apoptosis induced by ER stress was explored.Results1.In the apoptosis induced by ER stress,protein level of Cleaved-Caspase-3 increased significantly,while Hax-1 decreased dramatically.2.Overexpression of Hax-1 could lessen the production of apoptin,partly restrain apoptosis of cells induced by ER stress,and stabilize mitochondrial membrane potential(MMP).ConclusionOverexpression of Hax-1 partly restrain ER stress-induced apoptosis.更多还原