C57BL/6小鼠PD-1基因敲除后炎症与心房电重构的关系研究

PD-1 Deficiency Results in Atrial Electricity Remodeling in C57BL/6 Mice

目的:研究C57BL/6小鼠在PD-1基因敲除后体内炎症升高对房颤发病易感性的影响。方法:对两组动物进行了观察:C57BL/6小鼠和C57BL/6-PD-1基因敲除小鼠(各组均为15只,雄性,6-8周龄)。应用流式细胞仪微球芯片捕获技术对比了实验组与对照组的血清炎性细胞因子表达水平,应用多导电生理记录仪检测了实验组与对照组心房有效不应期和有效不应期离散度。结果:和对照组相比较,C57BL/6-PD-1-/-小鼠血清炎性细胞因子水平明显升高,C57BL/6-PD-1-/-小鼠心房肌有效不应期较对照组减低,而有效不应期离散度则明显升高。结论:PD-1基因敲除后出现的机体内炎性细胞因子水平的升高导致了C57BL/6小鼠的心房电重构,并由此使得C57BL/6-PD-1-/-小鼠心房纤颤发病易感性升高。

Objective： To investigate the effect of PD-1 deficiency in the pathogenesis of atrial fibrillation. Methods： Two groups of mice were used to carry out our experiment： C57BL/6 group（15 mice, male, 6-8 weeks） and C57BL/6-PD-1-/- group（15 mice, male,6-8 weeks）, the expression of inflammatory cytokines： interleukin（IL）-2,（IL）-4,（IL）-6,（IL）-10,（IL）-17, interferon（IFN）-γ and tumor necrosis factor（TNF）were determined by cytometric bead array, the atrial effective refractory period（AERPs） were determined by more conductive physiological recorder. Results： Inflammatory cytokines increased significantly in the PD-1-/-group compared with that in the C57BL/6 group; Mean while, the PD-1-/-group presented a shorter atrial effective refractory period and an increased dAERP. Conclusion：The higher level of inflammatory cytokines in the PD-1-/-mice results in atrial electricity remodeling in C57BL/6 mice, which lead to atrial fibrillation.