The Influence And Mechanism Of N-acetyl Cysteine On Rat Myocardial Fibrosis Induced By Pressure Overload

Objective:Hypertensive myocardial remodeling is the pathophysiological basis of hypertensive diseases and eventually results in heart failure. Myocardial fibrosis is closely connected to myocardial remodeling. Oxidative stress has a important role in the cardiopathogenesis of the HF. N-acetyl cysteine(NAC) is a free radical scavenger antioxidant.But the mechanisms of myocardial fibrosis in the pressure-overloaded heart.We will study the role of NAC in the myocardial fibrosis.Methods:1. Pressure-overloaded rat model is establishmented:Using common method by abdominal aortic coarctation(AAC) to establish pressure-overloaded rat model, after AAC 6 weeks for medical intervention.2. Group:(1)sham group;(2)sham+ N-acetyl cysteine(NAC) group;(3)AAC group;(4)AAC+ NAC group;3. Cardiac tissue weighing:The weight of the heart was weighed by electronic balance,and the records were recorded and analyzed statistically.4. Masson staining and immunohitochemistry:per sample was used to masson staining and immunohistochemistry.The Image-Pro Plus software and Axio Scope A1 were used to obverse myocardial fibrosis.Results:Contrasted with the model control group,AAC can induce the expression of TGF,NAC can reduce this change, with statistical significance; AAC group of heart weight increase, NAC can reduce the weight of the heart, with statistical significance; ACC can induce myocardial fibrosis, with statistical significance. Compared with the ACC group,NAC decreased myocardial fibrosis was not statistically significant, but there was a trend of NAC+AAC to reduce myocardial fibrosis.Conclusion:Inhibitting the expression of TGF/Smad signaling pathways, NAC can reduce myocardial fibrosis, improve ventricular remodeling. So the NAC to treatment of ventricular remodeling and myocardial fibrosis induced by pressure overload provides a new strategy.