前列腺素F2α诱导心肌细胞肥大效应的实验研究

Cardiomyocyte hypertrophy induced by PGF2α

目的观察前列腺素F2α（PGF2α）对心肌细胞内活性氧（ROS）的产生及其促心肌细胞肥大的作用，探讨ROS在PGF2α诱导的心肌细胞肥大的信号通路中的作用。方法细胞内ROS水平用ROS敏感的荧光探针（DCFH—DA）反映，心肌细胞肥大通过细胞内蛋白含量及细胞的直径大小来确定。结果用1nmol／LPGF2α、10nmol／LPGF2α、100nmol／LPGF2α诱导心肌细胞，其细胞内DCF—DA荧光强度值分别比对照组增加38、99％、61．76％、93．55％（F=195．69，P〈0．01），表明PGF2α可剂量依赖地诱导培养大鼠心肌细胞内ROS的产生；其蛋白含量分别比对照组增加39．51％、69．93％、139．06％（F=74．014，P〈0．01），其细胞直径分别比对照组增加29．02％、60．79％、127．40％（F=721．02，P〈0．01），表明PGF2α可剂量依赖地诱导培养大鼠心肌细胞的肥大。讨论PGF2α可剂量依赖地诱导培养大鼠心肌细胞内ROS的产生与心肌细胞的肥大。

Objective The effects of PGF2α on the reactive oxygen species generation and cardiomyocyte hypertrophy were examined in experiments on the cultured neonatal rat cardiomyocytes. It is to study the role of ROS in the signaling pathway of cardiomyocyte hypertro- phy induced by PGF2α. Methods The level of intracellular ROS was measured by the ROS-specific probe 2＇ ,7＇-dichlorofluorescin diacetate （DCF-DA）. Cardiomyocyte hypertrophy was determined by total protein content of the cells and the cell diameter. Results In the cardio- myocytes treated with PGF2α （ 1 nmol/1, 10nmol/1, 100nmol/l）, the fluorescence intensity of intracellular DCF-DA increased by 38. 99% , 61.76% and 93.55% respectively compared with control group （ F = 195. 69, P 〈0. 01 ）. It is indicated that PGF2αcan induce intracellu- lar ROS generation on the cultured neonatal rat cardiomyocytes in a dose-dependent manner. Compared with control group, the total protein increased by 39. 51%, 69. 93% and 139. 06% respectively （ F = 74. 014, P 〈 0. 01 ）, and the cell diameter increased by 29.02%, 60. 79% and 127.40% respectively （ F =721.02, P 〈0.01 ）. It is indicated that PGF2αinduce cardiomyocyte hypertrophy on the cultured neonatal rat cardiomyocytes in a dose-dependent manner. Conclusion PGF2αcan induce intracellular ROS generation and cardiomyocyte hypertrophy on the cultured neonatal rat cardiomyocytes in a dose-dependent manner.