摘要
目的:观察U83836E对原代大鼠心肌细胞缺氧复氧损伤的保护作用并探讨其初步机制。方法:分离大鼠原代心肌细胞建立缺氧复氧(H/R)模型,细胞随机分为5组,观察不同剂量U83836E对心肌细胞缺氧复氧损伤的保护作用。结果:与Control组比较,H/R组心肌细胞内钙离子浓度明显增高,肌浆网Ca^(2+)-ATP酶(SERCA2)表达显著减少。与H/R组比较,U83836E干预各组心肌细胞内游离钙离子浓度明显降低,且肌浆网钙泵的蛋白表达上调。结论:U83836E对缺氧复氧心肌细胞有保护作用,其可能与上调SERCA2的表达抑制细胞内钙超载有关。
Objective：The aim of this study was to investigate the protective effect and mechanism of U83836 Eagainst hypoxia/reoxygenation（H/R）injury on rat neonatal cardiomyocyte.Methods：Rat myocardial cells were cultured and divided into 5groups randomly.Then the hypoxia/reoxygenation（H/R）models were set up.The dissociative calcium concentration of myocardial cells with Fura2/AM fluorescent probe was measured and the content of the sarco/endoplasmic reticulum Ca^2＋-ATPases（SERCA2）were determined by Western blot method in each group.Results：The dissociative calcium concentration of the H/R group was much higher than that of the control group（P〈0.01）.However the expression of the SERCA2 in the H/R myocardial cells was lower than that of normal cells（P〈0.01）.U83836 Ecan lessen the calcium overload of cells and enhance the SERCA2 expression of the H/R myocardial cells（P〈0.05,P〈0.01）.Conclusion：U83836Ecan protect the H/R myocardial cells by attenuating the calcium overload and the mechanism is probably enhance the expression of SERCA2.
出处
《长治医学院学报》
2016年第4期241-244,共4页
Journal of Changzhi Medical College
基金
长治医学院科技创新团队项目(CX201409)
山西省高等学校"131"领军人才工程项目
关键词
心肌细胞
缺氧复氧
钙超载
肌浆网CA^2+-ATP酶
cardiomyoctyes
hypoxia/reoxygenation
calcium overload
sarco/endoplasmic reticulum Ca2＋-ATPases（SERCA2）
