Effect of Candesartan Combined with Rosuvastatin on Myocardial Fibrosis in Rats with Alcoholic Cardiomyopathy by Mediating LOX-1 Expression

Abstract

Objective: To analyze the effect of candesartan and rosuvastatin on myocardial fibrosis in rats with alcoholic cardiomyopathy by mediating the expression of lectin-like oxidized low-density lipoprotein receptor-1(LOX-1). Methods: The rats were selected as experimental samples, and these rats were randomly divided into observation group and alcohol feeding group (abbreviated as "alcohol group") and desartan combined with rosuvastatin intervention + alcoholic cardiomyopathy group (Referred to as the "intervention group"), the observation group is fed normally, the alcohol group is fed with alcohol, and the intervention group uses two drugs on the basis of the alcohol group to intervene. After 16 weeks of the three groups of experiments, analyze the results of the three groups of experiments. Myocardial structure, myocardial fibrosis and myocardial function. Results: After 16 weeks, the left ventricular short axis shortening rate (FS) and left ventricular ejection fraction in the alcohol group were lower than those in the observation group, while the collagen volume fraction (CVF) and left ventricular end-diastolic diameter (LVEDd) were higher than those in the observation group. The expression of LOX-1 in the intervention group was lower than that in the alcohol group, and the degree of fibrosis was reduced. The expression of LOX-1 in the alcohol group was higher than that in the observation group, and the degree of fiber increased. At the same time, the expression of TN-X and smad-3 protein in the alcohol group (86%± 7%, 83%±9%) were higher than those in the observation group (32%±10%, 30%±7%), while the expression of smad-7 protein (36%±8%) was lower than that in the observation group (78%± 9%), P<0.05 among the three groups of experiments, and there is statistical significance among the groups. Conclusion: Candesartan combined with Rosuvastatin can reduce myocardial fibrosis in rats with alcoholic cardiomyopathy by mediating the expression of LOX-1.