Search

Objective: To investigate the effects of sacubitril/valsartan on the expression of Galectin-3 (Gal-3) and Matrix metalloproteinase-9 (MMP-9) in New Zealand rabbits with stressinduced cardiac hypertrophy. Methods:Twenty-four healthy male 8-week-old New Zealand rabbits were randomly divided into sham operation group (Sham), model group (Model), and sacubitril/valsartan group (Sacu/Vals), with 8 rats in each group. Abdominal aortic coarctation was used to construct a model of cardiac hypertrophy. After 8 weeks of successful modeling, the acubitril/valsartan group was administered with the drug, and the other two groups were given an equal volume of normal saline. All rabbit hearts were sacrificed at the end of the 16th week. The left ventricular mass index and the whole heart mass index were measured. The left ventricular myocardial tissue was evaluated by HE staining to evaluate the cardiac hypertrophy. The expression of Gal-3 and MMP-9 in the myocardial tissue was detected by western blot. Results: (1) Compared with the sham operation group, the HMI and LVMI of the model group and the sacubitril/valsartan group increased. Compared with the model group, the HBA and LVMI decreased in the sacubitril/valsartan group; (2) In the sham operation group, the myocardial fibers were arranged neatly, arranged in a bundle, and the morphology was intact, and no obvious fibrous tissue was observed. The myocardial fibers in the model group were disordered, most of them were broken, the cells were edematous, and the myocardial interstitial showed fibrous connective tissue. Compared with the model group, the sacubitril/valsartan group had a neat arrangement of myocardial fibers and a significant reduction in cell edema; (3) Compared with sham operation, the expression of Gal-3 and MMP-9 protein in the model group and the sacubitril/valsartan group increased; compared with the model group, sacubitril/valsartan the expression levels of Gal-3 and MMP-9 in the tan group were decreased. Conclusion: Sacubitril/valsartan can alleviate cardiac hypertrophy in rabbits, and its mechanism may be related to down-regulation of Gal-3 and MMP-9 protein expression.