论文部分内容阅读
目的:探讨辛伐他汀是否通过抑制心肌细胞的钠氢交换保护心肌急性氧化损伤。方法:用可标记pH值的荧光探针SNARF-1和可标记Ca~(2+)的荧光探针Fluo-3/AM同时负载原代培养的乳鼠心肌细胞30 min,先后加入H_2O_2及辛伐他汀等药物,激光共聚焦显微镜检测,根据荧光探针被激发出的不同颜色的荧光强度,同步绘出细胞内pH值(pHi)和细胞内钙离子浓度([Ca~(2+)]i)的变化趋势图。结果:辛伐他汀使H_2O_2引起的pHi和[Ca~(2+)]i上升分别下降0.08±2.28和0.16±0.53(P<0.05),与阿米洛利(EIPA)的作用相似。结论:辛伐他汀能通过影响心肌细胞内的钠氢交换快速起效,使细胞内pH值下降,抑制钙超载,从而对心肌的氧化损伤起急性保护功能。
Objective: To investigate whether simvastatin can protect myocardium from acute oxidative damage by inhibiting the exchange of sodium and hydrogen in myocardial cells. Methods: Primary cultured neonatal rat cardiomyocytes were loaded with fluorescence probe labeled with SNARF-1 and Fluo-3 / AM labeled with Ca 2+ for 30 min. H 2 O 2 According to the fluorescence intensities of different colors excited by the fluorescent probe, the intracellular pH (pHi) and the intracellular calcium concentration ([Ca2 +]) were plotted synchronously by laser scanning confocal microscopy, i) the trend of change. Results: Simvastatin decreased the pHi and [Ca ~ (2 +)] i induced by H_2O_2 by 0.08 ± 2.28 and 0.16 ± 0.53, respectively (P <0.05), similar to that of Etimiamide (EIPA). Conclusion: Simvastatin can exert rapid onset of cardiomyocyte sodium and hydrogen exchange, decrease intracellular pH and inhibit calcium overload, thereby protecting myocardium from oxidative damage.