| BackgroundHeart failure remains one of the most prevalent and challenging medical conditions. Recent studies showed galectin-3played an important role in the pathophysiology of heart failure. The cholesterol-lowering statin drugs have some non-lipid-lowering effects, such as inhibiting myocardial remodeling. However, the underlying mechanism is still unclear. Our aims are to study the association between plasma galectin-3levels and heart failure after myocardial infarction and to evaluate the clinical prognostic value of plasma galectin-3in patients with heart failure and the intervention role of atorvastatin.MethodsThe left anterior descending coronary artery was ligated to establish a rat model of heart failure, and the rats were divided into a sham operation (Sham) group, myocardial infarction model (MI) group, and MI-atorvastatin group. Changes in hemodynamic parameters were recorded after the final drug administration. Histological diagnosis was by reviewing hematoxylin and eosin (H&E) stained tissue. Real-time quantitative polymerase chain reaction (PCR) was performed to determine the expressions of type I and type III collagen, MMP-2, and TIMP-2. Further, primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of atorvastatin on cardiac fibroblast proliferation.ResultsWith the deterioration of cardiac function in patients, Galectin-3was gradually increased. The model of heart failure was established and the results of HE staining and Masson’s trichrome staining revealed that the rats in MI model group showed obvious hyperplasia of fibrotic tissue, which was significantly reduced in the atorvastatin group. The results of real-time quantitative PCR showed that the expression of type I and type III collagen, MMP-2, and TIMP-2in the heart failure group were significantly increased, but MMP-2/TIMP-2ratio was significantly reduced, Compared with the heart failure group, the atorvastatin group showed significantly reduced expression of type I and III collagen, unchanged expression of MMP-2, significantly reduced expression of TIMP-2, and an increased MMP-2/TIMP-2ratio. We further found that atorvastatin can significantly inhibit the Ang II-induced fibroblast proliferation and the expression of type I and type III collagen in cardiac fibroblasts while increasing the MMP-2/TIMP-2ratio.Conclusions:In summary, Galectin-3could predict the incidence of heart failure after acute myocardial infarction. The data suggest that atorvastatin could inhibit cardiac fibroblast proliferation and enhance collagen degradation by increasing the MMP-2/TIMP-2ratio, thereby inhibiting the formation of myocardial fibrosis in rats with heart failure after myocardial infarction. |
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