Si-Miao-Yong-An decoction attenuates cardiac fibrosis via suppressing TGF-β1 pathway and interfering with MMP-TIMPs expression - 30/05/20
, Shuzhen Guo a, ⁎ , Wei Wang a, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Graphical abstract |
SMYAD attenuated cardiac fibrosis via decreasing collagen synthesis by suppressing TGF-β1 pathway and increasing collagen degradation by interfering with MMP-TIMPs expression.
Highlights |
• | SMYAD reduced fibrosis level and improved TAC-induced heart failure in mice. |
• | SMYAD attenuated cardiac fibrosis via decreasing collagen synthesis by suppressing TGFβ1/Smad pathway and increasing collagen degradation by interfering with MMP-TIMPs expression. |
• | Our study suggests the potential of SMYAD for the treatment of heart failure. |
Abstract |
Background |
Myocardial fibrosis is an important pathological feature of pressure overload cardiac remodeling. Si-Miao-Yong-An decoction (SMYAD), a traditional Chinese formula, is now clinically used in the treatment of cardiovascular diseases in China. However, its mechanisms in the prevention of heart failure are not fully revealed.
Purpose |
To determine whether treatment with SMYAD for 4 weeks would lead to changes in collagen metabolism and ventricular remodeling in a mice model of heart failure.
Methods |
Mice were subjected to transverse aorta constriction to generate pressure overload induced cardiac remodeling and then were administered SMYAD (14.85 g/kg/day) or captopril (16.5 mg/kg/day) intragastrically for 4 weeks after surgery. Echocardiography and immunohistochemical examination were used to evaluate the effects of SMYAD. The mRNA of collagen metabolism biomarkers were detected. Protein expression of TGF-β1/Smad and TGF-β1/TAK1/p38 pathway were assessed by Western blot.
Results |
SMYAD significantly improved cardiac function, increased left ventricle ejection fraction, and decreased fibrosis area and αSMA expression. Moreover, SMYAD reduced proteins expression related to collagen metabolism, including Col1, Col3, TIMP2 and CTGF. The increased levels of TGF-β1, Smad2, and Smad3 phosphorylation were attenuated in SMYAD group. In addition, SMYAD reduced the levels of TGF-β1, p-TAK1 and p-p38 compared with TAC group.
Conclusions |
SMYAD improved cardiac fibrosis and heart failure by inhibition of TGF-β1/Smad and TGF-β1/TAK1/p38 pathway. SMYAD protected against cardiac fibrosis and maintained collagen metabolism balance by regulating MMP-TIMP expression. Taken together, these results indicate that SMYAD might be a promising therapeutic agent against cardiac fibrosis.
Le texte complet de cet article est disponible en PDF.Abbreviations : HF, SMYAD, TAC, EF, FS, HE, ECM, MMP, TIMP, CTGF
Keywords : Si-Miao-Yong-An decoction, Cardiac fibrosis, Transverse aorta constriction, TGF-β, Matrix metalloproteinase
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Vol 127
Article 110132- juillet 2020 Retour au numéro
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