论文部分内容阅读
目的观察KATP通道开放剂吡那地尔对缺血缺氧PC12细胞凋亡的影响,探讨KATP通道开放剂对缺血缺氧PC12细胞凋亡的信号转导机制。方法取传代后3d的PC12细胞,分为正常对照组、缺血对照组、吡那地尔预处理组、吡那地尔+格列吡嗪处理组共4组。采用Annexin-VFITC/PI双染流式细胞分析仪检测凋亡率,应用Western-blotting检测p-CREB蛋白表达水平,观察KATP开放剂对缺血缺氧PC12细胞凋亡的保护作用。结果与缺血对照组相比,吡那地尔预处理组PC12细胞凋亡率明显降低(p<0.05),吡那地尔预处理组PC12细胞p-CREB蛋白表达增加(p<0.05)。结论 KATP通道开放剂吡那地尔能明显降低缺血缺氧后PC12细胞凋亡,增加p-CREB蛋白表达,CREB可能是KATP通道开放剂减少缺血缺氧后PC12细胞凋亡的途径之一。
Objective To observe the effect of pinacidil, a KATP channel opener, on the apoptosis of hypoxic-ischemic rat PC12 cells and to explore the signal transduction mechanism of KATP channel opener on the apoptosis of hypoxic-ischemic rat PC12 cells. Methods The PC12 cells after passage 3 days were divided into 4 groups: normal control group, ischemia control group, pinacidil pretreatment group, pinacidil + glipizide treatment group. The apoptotic rate was detected by Annexin-VFITC / PI double staining flow cytometry. The expression of p-CREB protein was detected by Western-blotting. The protective effect of KATP opener on the apoptosis of hypoxic-ischemic rat PC12 cells was observed. Results Compared with the ischemic control group, the apoptosis rate of PC12 cells in the pinacidil preconditioning group was significantly decreased (p <0.05). The expression of p-CREB protein in the PC12 cells in the pinacidil preconditioning group was increased (p <0.05). Conclusions Pinagnaine, a KATP channel opener, can significantly reduce the apoptosis of PC12 cells and increase the expression of p-CREB protein after hypoxia-ischemia, and CREB may be one of the pathways of KATP channel opener to reduce the apoptosis of PC12 cells after hypoxia-ischemia .