摘要
目的观察UcnⅠ对成年大鼠缺氧/复氧损伤心肌细胞钙离子的影响。方法通过Langendorff离体心脏灌注系统,用Ⅱ型胶原酶逆行灌注法分离成年大鼠心肌细胞,培养20 h后随机分为正常组(N组)、缺氧/复氧组(I/R组)、UrocortinⅠ组(UcnⅠ组)、5-羟葵酸+UrocortinⅠ组(5-HD+UcnⅠ组)。各处理组心肌细胞加入Fluo-3/AM荧光探针,用激光共聚焦显微镜检测细胞内钙的荧光强度。结果 I/R组心肌细胞内钙离子浓度较N组高(P<0.05),UcnⅠ组较N组荧光强度明显增强(P<0.01),而5-HD+UcnⅠ组心肌细胞内钙离子荧光强度与UcnⅠ组比较明显降低(P<0.05)。结论 UcnⅠ可使成年大鼠缺氧/复氧损伤心肌细胞内钙离子浓度升高,5-HD则可阻断UcnⅠ的作用,提示UcnⅠ导致缺氧/复氧后心肌细胞钙离子浓度的升高可能跟ATP敏感性钾通道开放有关。
Objective To investigate the effects of Urocortin I（UcnⅠ） on calcium concentration of cultured adult rat cardiomyocytes after hypoxia/reoxygenation injury.Methods Adult rat cardiomyocytes were separated and cultured by type II collagenase retrograde perfusion using Langendorff isolated heart perfusion apparatus.Twenty hours later,the cardiomyocytes cells were randomly divided into normal group（N）,hypoxia/reoxygenation group（I/R）,UrocortinⅠgroup（UcnⅠ） and 5-HD＋UrocortinⅠgroup（5-HD＋ UcnⅠ）.The cultured cardiomyocytes were mixed with Fluo-3/AM fluorescent probe and the calcium concentrations of cultured cardiomyocytes were detected via the confocal microscope.Results The inflorescence intensity of intracellular calcium in I/R and Ucn I groups was higher than that in N group（P0.05）.However,the inflorescence intensity of intracellular calcium in 5-HD＋UcnⅠgroup was much lower than that in UcnⅠgroup（P0.05）.Conclusion 5-HD could block Ucn I-induced increase of intracellular calcium concentration in the cultured adult rat cardiomyocytes after hypoxia/ reoxygenation injury,suggesting that Ucn I-increased calcium concentration in hypoxia/reoxygenation-injured cardiomyocytes might be related to ATP sensitive potassium channel opening.
出处
《遵义医学院学报》
2012年第3期193-195,共3页
Journal of Zunyi Medical University
基金
贵州省科学技术基金项目(NO:黔科合J字[2008]2196)
遵义医学院科研启动基金(NO:[2010]448)
