Simvastatin inhibits ROS mediated the neonatal rat cardiac myocyte hypertrophy induced by endothelin-1 / 中国药理学通报

ABSTRACT

AIM To explore the inhibitory effects of simv astatin on ROS generation and cardiac myocytes hypertrophy induced by ET-1. METHODS The study was performed with primary cultured neonatal rat cardiac myocytes. Intrace llular fluorescence signal was assayed by fluorescence convert microscope. The l evel of intracellular ROS was measured by the ROS-specific probe 2′, 7′-dich lorofluorescin diacetate (DCF-DA). The RNA content was determined by RNA-sensitive fluoresce nce probe propidium iodide (PI) and the total protein of cell was measured by th e methods of coomassie brilliant blue. The cell surface area was measured by ima ge analysis program. RESULTS ①Fluorescence intensity of intracel lular DCF-DA and myocyte hypertrophy increased by ET-1 in dose-dependent mann er. Antioxidant catalase(0 2 U?L -1 ) attenuated the ET-1-induced incre ase of fluorescence intensity of intracellular DCF-DA and myocyte hypertrophy.②Simvastatin inhibited the increase of fluorescence intensity of intracellular DCF-DA and cardiac myocyte hypertrophy induced by ET-1(10 -8 mol?L -1 )in a dose-dependent manner. CONCLUSION ET-1 increases int racellular ROS in the cultured neonatal rat cardiac myocytes. Simvastatin inhibi ted the generation of ET-1-induced ROS and cardiomyocytes hypertrophy.