碘化N-正丁基氟哌啶醇对缺氧复氧内皮细胞早期生长反应基因-1表达的影响  

Effect of N-n-butyl Haloperidol Iodide on Egr-1 Expression of Endothelial Cells Induced by Hypoxia and Reoxgenation

作　　者：周燕琼[1,2] 张艳美[1] 高分飞[1] 黄展勤[1] 陈一村[1] 王锦芝[3] 蔡文峰[1] 郑燕珊[1] 石刚刚[1] 

机构地区：[1]汕头大学医学院药理学教研室,广东汕头515041 [2]汕头大学医学院第二附属医院药学部,广东汕头515041 [3]汕头大学医学院化学教研室,广东汕头515041

出　　处：《汕头大学医学院学报》2012年第3期132-134,137,F0002,共5页Journal of Shantou University Medical College

基　　金：国家自然科学基金委员会-广东省人民政府自然科学联合基金资助项目(U0932005);国家自然科学基金资助项目(811-73048;81072633);汕头市科技计划资助项目(汕府科[2010]63号)

摘　　要：目的:观察碘化N-正丁基氟哌啶醇(F2)对缺氧复氧(H/R)条件下大鼠心脏微血管内皮细胞(RCMECs)早期生长反应基因-1(Egr-1)表达的影响。方法:体外培养RCMECs,建立其H/R模型。细胞随机分为对照组,H/R组,溶剂(PEG)组和F2组。在细胞缺氧3 h复氧2h后收集细胞及上清液,免疫细胞化学法检测细胞中Egr-1蛋白的表达水平,显微镜下观察细胞形态学改变并计算存活率。结果:H/R及PEG组内皮细胞在H/R刺激下Egr-1蛋白表达明显升高,细胞形态发生改变,存活率降低。F2组的内皮细胞在H/R刺激下Egr-1的异常表达受抑制,细胞形态结构无明显改变,细胞存活率提高。结论:F2对体外培养的RCMECsH/R损伤具有保护作用,这可能与其抑制Egr-1蛋白过表达有关。Objective： To study the effect of N-n-butyl haloperidol iodide（F2）on Egr-1 expression of rat cardiac microvascular endothelial cells（ RCMECs） induced by hypoxia and reoxgenation. Methods： RCMECs were cultured /n v/tro and the hypoxia-reoxgenation（H/R）model was established. Cells were divided at random into control, H/R, PEG and F2 groups. Cells and cultured supematants were collected after 3 hours hypoxia and 2 hours reoxgenation. Egr-1 expres- sion of endothelial cells was determined by immunocytochemical method. Cell morphology and cell viability were observed to assess the degree of injury. Results： In the H/R and PEG groups, the expression of egr-1 protein of RCMECs treated with H/R increased markedly. The cell morphology changed and cell survival was decreased. In the F2 group, egr-1 protein expression of RCMECs was down-regulated, the cell morphology and cell survival were improved. Conclusion： F2 can protect RCMECs from the injury of H/R, which might be related with the down-regulation of egr-1 protein expression.

关 键 词：碘化N-正丁基氟哌啶醇 内皮细胞 缺氧复氧 EGR-1 细胞存活率 

分 类 号：R322.124[医药卫生—人体解剖和组织胚胎学] R329.2[医药卫生—基础医学]