摘要
目的探讨干预NF-κB通路对划痕损伤后脑微血管内皮细胞增殖的影响。方法用划痕法建立大鼠脑微血管内皮细胞损伤模型,随机分成空白组、激活组、抑制组、划痕组、划痕+激活组、划痕+抑制组6组,其中激活组给予NF-κB激活剂佛波醇脂(PMA)干预,抑制组在吡咯醛二硫氨基甲酸(PDTC)预处理后加用PMA。各组细胞处理1、6、12、24、48 h后,免疫细胞荧光法测定磷酸化NF-κBp65表达,MTS法检测细胞增殖的情况。结果随着作用时间增加,除去空白组外其余组的NF-κB蛋白表达量逐渐增高,但抑制组NF-κB蛋白表达均较激活组明显减少。各组细胞均有不同程度增殖,其中激活组、划痕+激活组增殖最明显。结论 NF-κB信号通路激活可促进脑微血管内皮细胞增殖,而阻断NF-κB信号通路可抑制增殖。
Objective To investigate the effect of PMA and PDTC-interfered NF-κB signaling pathway on proliferation of scratched brain microvascular endothelial cells（BMECs）. Methods Rat BMECs were used to establish cell injury model by the scratch method and then randomly divided into blank, activation, inhibition, scratch, scratch ＋ activation and scratch ＋ inhibition groups. Activation and inhibition groups were treated with PMA and PDTC, respectively. Phosphorylated NF-κBp65 and proliferation at 1 h, 6 h, 12 h, 24 h and 48 h were detected by immunocytochemistry fluorescence method and MTS, respectively.Results Phosphorylated NF-κBp65 expression was gradually increased with the treatment time in all groups except blank group, but its expression was reduced in inhibition group compared with activation group. Each group showed different degrees of proliferation, especially in activation and scratch ＋ activation groups. Conclusion NF-κB signaling pathway activation enhances proliferation, while its blockade inhibits proliferation of BMECs.
出处
《广东医学院学报》
2015年第1期52-55,共4页
Journal of Guangdong Medical College
基金
2011年广东医学院附属医院优秀硕士学位论文培育计划项目(No.2011y08)
2012年广东医学院附属医院青年科研基金项目(No.Qk1308)
2013年广东医学院青年科研基金项目(No.XQ1315)
2013年广东医学院面上培育项目(No.[2013]9号)
