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Background: TGF-β/Smads and Wnt/β-catenin pathway are recognized as the most important myocardial fibrosis signaling pathway. Recent studies reported Salidroside(Salid) on the angiogenesis and apoptosis in liver fibrosis, while there was no evidence of Salid on preventing or reversing myocardial fibrosis and the underlying mechanism remain unclear.
Methods: After left anterior descending coronary artery ligation, rats received either intraperitoneal injection of Salid, or the same volume of saline. Cardiac function was assessed echocardiographically, and angiogenesis was assessed histologically four weeks after therapy.
Results: Sirius red staining showed that the ratio of collagen I/III in Salid group was significantly lower than that in model group. Western blot and RT-PCR analysis showed that the expression levels of P-Smad3 and Smad2/3 were down-regulated as well as DVL-1 and β-catenin in Wnt/β-catenin Pathway, Compared with the control group, the expression of Smad3 and β-catenin in the non-infarcted myocardium of the group were significantly lower. The number of Salid groups had a lower level of Gal-3 in the peripheral blood both on the 28th and the 56th day.
Conclusions: These results show for the first time that Salid can improve myocardial fibrosis in ventricular remodeling through the mechanism of regulation of TGF-β/Smads and Wnt/β-catenin pathway. The positive regulation of TGF-β by the crosstalk pathway of Smad3 and β-catenin may serve as a potential target for anti-fibrosis.
Poster Hall, Hall C
Saturday, March 18, 2017, 3:45 p.m.-4:30 p.m.
Session Title: Cardiac Fibrosis and Heart Failure: The Next Frontier
Abstract Category: 12. Heart Failure and Cardiomyopathies: Basic
Presentation Number: 1249-260
- 2017 American College of Cardiology Foundation