中文摘要：

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（Sgr-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3h复氧2h后收集细胞及上清液，免疫细胞化学法检测细胞中Eg-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：R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。

英文摘要：

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.