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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 observe the expression of Egr-1 in rat cardiac microvascular endothelial cells (RCMECs) under hypoxia-reoxygenation (H / R) condition with Nn-butyl haloperidol iodide (F2) Impact. Methods: RCMECs were cultured in vitro and their H / R model was established. The cells were randomly divided into control group, H / R group, solvent (PEG) group and F2 group. The cells and supernatants were harvested 2 hours after reoxygenation for 3 hours and the expression of Egr-1 protein was detected by immunocytochemistry. Morphological changes were observed under microscope and the survival rate was calculated. Results: The Egr-1 protein expression in H / R and PEG-treated groups was significantly increased after H / R stimulation. The morphological changes of cells and the decrease of survival rate were observed. The abnormal expression of Egr-1 in endothelial cells of F2 group under H / R stimulation was inhibited, the morphology and structure of the cells were not changed, and the cell survival rate was increased. CONCLUSION: F2 has a protective effect on H / R injury induced by RCMECs in vitro, which may be related to the inhibition of Egr-1 protein overexpression.