节点文献
碘化N-正丁基氟哌啶醇对培养大鼠心肌细胞缺氧复氧损伤及Egr-1表达的影响
Effects of N-n-butyl haloperidol iodide on hypoxia/reoxygenation injury and Egr-1 expression in cultured rat cardiomyocytes
【摘要】 目的观察碘化N-正丁基氟哌啶醇(F2)对培养大鼠心肌细胞缺氧复氧(H/R)所致的损伤及早期生长反应蛋白-1(Egr-1)表达变化的影响。方法制作心肌细胞H/R损伤模型。倒置显微镜和透射电子显微镜下观察心肌细胞一般形态、自发性搏动及超微结构的变化。采用免疫组织化学方法测定心肌细胞Egr-1蛋白阳性表达的细胞数。结果H/R造成心肌细胞形态异常、搏动节律紊乱,导致超微结构损害;H/R诱导心肌细胞Egr-1表达明显增强。缺氧及复氧前给予F2则能改善H/R所致心肌细胞病理损害,抑制心肌细胞Egr-1的过量表达。结论F2对培养心肌细胞H/R损伤具有保护作用,这可能与其抑制Egr-1蛋白过量表达有关。
【Abstract】 Objective To investigate the relationship between the protective effects of N-n-butyl haloperidol iodide(F2) on hypoxia/reoxygenation(H/R) injury and the expression of early growth response(Egr-1) in cultured rat cardiomyocytes.Methods The H/R models of neonatal rat cardiomyocytes were established.The changes of morphology,spontaneous beat and ultrastructure of cardiomyocytes were detected by inverted microscope and transmission electron microscope.The numbers of Egr-1-immunopositive cell were counted by immunohistochemistry.Results H/R caused cultured cardiomycyte paramorphia,arrhythmic beat and ultrastructural damage.H/R induced strong expression of Egr-1 in cardiomycytes.Treatment with F2 before hypoxia and reoxygenation significantly attenuated the cardiomyocytes injury and inhibited the overexpression of Egr-1 after H/R.Conclusion F2 can protect cultured cardiomycytes from H/R injury,which might be associated with the inhibition of Egr-1 overexpression.
【Key words】 Haloperidol; Early growth response-1; Cardiomyocytes; Hypoxia; Reoxygenation;
- 【文献出处】 山西医药杂志 ,Shanxi Medical Journal , 编辑部邮箱 ,2006年07期
- 【分类号】R541
- 【下载频次】104