氟桂利嗪对缺血再灌注后PC12细胞质钙离子浓度和核转录因子表达影响的研究

目的　观察氟桂利嗪对缺血再灌注损伤中PC12细胞质Ca2 + 浓度的变化和核转录因子 (NF κB)表达的影响。方法　将传代培养的PC12细胞在特制的装置中进行缺血再灌注处理 (单纯缺血再灌注组 ) ,建立研究所需要的细胞模型并施以氟桂利嗪进行干预 (氟桂利嗪处理组 ) ,运用激光共聚焦显微镜检测不同处理条件下细胞质的Ca2 + 浓度 ,并应用免疫细胞化学和流式细胞仪技术对NF κB的表达情况进行检测。结果　氟桂利嗪处理组与单纯缺血再灌注组比较 ,细胞质Ca2 + 浓度和NF κB的表达均有降低。结论　氟桂利嗪能够减少缺血再灌注引起的细胞质PC12细胞Ca2 + 和NF κB的上调 ,可能具有细胞保护性作用 ;缺血再灌注损伤中NF κB的激活可能存在着Ca2 + 调控通路。

Effects of flunarizine on intracellular Ca2+ and NF-κB in PC12 cells following ischemia-reperfusion injury

Objective To observe the effects of flunarizine on intracellular Ca 2+ and NF-κB in PC12 cells following ischemia-reperfusion injury. Methods The subcultured PC12 cells were subjected to ischemia-reperfusion injury(control group) and were pretreated with flunarizine(flunarizine-treated group) in a special device. The changes of the concentration of Ca 2+ under different conditions were measured by confocal laser scanning microscope, and the expression of NF-κB was measured by immunocytochemistry and flow cytometer.Results Both the concentration of Ca 2+ and the expression of NF-κB in the flunarizine-treated group were lower than those in the control group.Conclusions It was probable that flunarizine could protect PC12 cells from ischemia-reperfusion injury by down-regulating the increased intracellular Ca 2+ and NF-κB induced by ischemia-reperfusion,and intracellular Ca 2+ might modulate the activation of NF-κB induced by ischemia-reperfusion injury in PC12.