Objective:Endothelial nitric oxide synthase(eNOS)and nitric oxide(NO)have been implicated to protect myocardial ischemia injury. However,the angiogenic effect of eNOS in infarcted myocardium and the role of MAPK signaling in eNOS/NO-mediated cardiac remodeling have not yet been elucidated. We observed the cardioprotective effects of eNOS gene transfection after myocardial infarction. Methods:Wistar rats(male) were divided into short-term group(24-hour infarction) for signaling investigations and long-term group(7-day infarction) for ventricular remodeling. Human eNOS gene in an adenovirus vector was delivered locally into rat heart 4 days prior to induction of myocardial infarction(MI) by left anterior descending coronary artery ligation. Cardiomyocyte inflammation was detected by immunohistochemistry. Expression of MAPKs were detected by Western Blot. Results:eNOS gene transfection significantly reduced myocardial infarct size and improved cardiac contractility as well as left ventricle(LV) diastolic function after MI. In addition,eNOS significantly reduced MI-induced cardiomyocyte inflammation. Activation of JNK and P38 after MI were also dramatically reduced by eNOS. Moreover,the deterioration of both systolic and diastolic function in conjunction with thin LV remodeling after MI were prevented by eNOS. Conclusion:These results demonstrate that the eNOS/NO system provides cardiac protection after MI injury through inhibition of cardiac inflammation and suppression of JNK and P38 signaling. The resule that all the cardioprotective effects of eNOS were blocked by N(-棕)-nitro-L-arginine methyl ester administration indicates a NO-mediated event.