摘要
Background Aldosterone blockers could reduce the incidence of ventricular arrhythmias in myocardial infarction（MI） patients by regulating hyperpolarization-activated cyclic nucleotide-gated channel（HCN） expression.But the mechanism underling HCN expression is unclear.Methods Eighteen rats surviving 24 hours postMI were randomly divided into 3 groups：MI,spironolactone,and spironolactone ＋ antagomir-133（mi RNA-133suppression）.Sham group rats had a suture loosely tied around the left coronary artery,without ligation.HCN2 and HCN4 protein and m RNA level,and mi RNA-133 level in the border zone of post-MI 1 week myocardium were measured.Results Spironolactone significantly increased mi RNA-133 levels and down-regulated HCN2 and HCN4 at both m RNA and protein levels in post-MI border zone myocardium.Antagomir-133 reduced the effects of spironolactone on HCN2 and HCN4 protein levels.Conclusions The results suggest that mi RNA-133 is involved in spironolactone induced HCN expression,and partially contributed to post-MI ventricular arrhythmias.
Background Aldosterone blockers could reduce the incidence of ventricular arrhythmias in myocardial infarction（MI） patients by regulating hyperpolarization-activated cyclic nucleotide-gated channel（HCN） expression.But the mechanism underling HCN expression is unclear.Methods Eighteen rats surviving 24 hours postMI were randomly divided into 3 groups：MI,spironolactone,and spironolactone ＋ antagomir-133（mi RNA-133suppression）.Sham group rats had a suture loosely tied around the left coronary artery,without ligation.HCN2 and HCN4 protein and m RNA level,and mi RNA-133 level in the border zone of post-MI 1 week myocardium were measured.Results Spironolactone significantly increased mi RNA-133 levels and down-regulated HCN2 and HCN4 at both m RNA and protein levels in post-MI border zone myocardium.Antagomir-133 reduced the effects of spironolactone on HCN2 and HCN4 protein levels.Conclusions The results suggest that mi RNA-133 is involved in spironolactone induced HCN expression,and partially contributed to post-MI ventricular arrhythmias.
基金
National Natural Science Foundation of China(No.NSFC81100088)
