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Published:
Aug 10, 2022DOI:
10.4314/tjpr.v21i6.3Keywords:
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Main Article Content
S-adenosyl-L-methionine improves ventricular remodeling after myocardial infarction by regulating angiogenesis and fibrosis
Abstract
Purpose: To investigate the effect of S-adenosyl-L-methionine (SAM) on angiogenesis and fibrosis in the heart of rats with myocardial infarction (MI), and to determine the mechanism of action.
Methods: Sprague Dawley rats with MI received SAM treatment (15 mg/kg) intraperitoneally. The cumulative survival (%) of rats was recorded to determine their rate of survival. Hematoxylin-eosin staining, echocardiography, and hemodynamics were also performed. In addition, the effects of SAM vascular regeneration in the rats were analyzed by determining the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and hypoxia-inducible factor 1-α (HIF1-α) in rats.
Results: The 8-week survival rate of the MI group was significantly lower than that of the sham group, while SAM significantly improved the survival rate of the rats. In addition, SAM improved the contractile and diastolic heart function in the rats and also increased the ventricular pressure change. Furthermore, SAM elevated the expressions of VEGF, bFGF and HIF1-α in rat myocardium and serum. In myocardial tissues of SAM-treated rats, the expressions of collagen I, collagen III and α-sma were reduced, indicating that SAM inhibited myocardial fibrosis. In addition, SAM promoted cardiac angiogenesis by activating Jagged1/Notch1 signaling pathway.
Conclusion: SAM promotes angiogenesis of the myocardium by activating Jagged1/Notch1 signaling pathway and inhibiting fibrosis in rat myocardium. Therefore, SAM effectively inhibits ventricular remodeling in rats after MI, thereby improving the rats’ heart structure and function. The results may provide new targets for the treatment of myocardial infarction.
