Abstract

Purpose: To investigate the remodeling influence of salidroside (SAL) on the ventricles following acute myocardial infarction (AMI) in rats, and the processes involved.Methods: A total of 65 Sprague Dawley (SD) rats were assigned to 5 groups: sham (n = 13), model, and low-, medium- and high-dose SAL groups given SAL at doses of 12, 34, and 36 mg/day, respectively, with 13 rats in each group. Changes in pathological structure, collagen area, ratio of collagen I/collagen III, left ventricular mass index (LVW/BW), ratio of cardiac weight to body weight (HW/BW), creatine kinase MB isoenzyme (CK-MB), lactate dehydrogenase-1 (LDH-1), endothelin (ET), laminin (LN), and hyaluronic acid (HA) were evaluated. Expression levels of dishevelled-1 (DVL-1) and β-catenin in myocardial tissues of the rats were also determined.Results: The LVW/BW values were significantly higher in the low SAL and medium SAL groups than those in AMI rats, while the ratio of collagen I/III and expression levels of DVL-1 and β-catenin proteins were significantly lower than those in the model group (p < 0.05). The myocardial structure of rats in the sham group was normal, with no obvious lesions. The levels of CK-MB, LDH-1, ET, LN, and HA in medium and high-dose SAL groups were significantly lower than those in the model group (p < 0.05).Conclusion: Salidroside mitigates remodeling of ventricles following AMI in rats by modulating the Wnt/β-catenin signal route.

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