Si-Miao-Yong-An Decoction attenuates isoprenaline-induced myocardial fibrosis in AMPK-driven Akt/mTOR and TGF-?/SMAD3 pathways - 27/10/20
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Abstract |
Myocardial fibrosis is well-known to be the aberrant deposition of extracellular matrix (ECM), which may cause cardiac dysfunction, morbidity, and death. Traditional Chinese medicine formula Si-Miao-Yong-An Decoction (SMYAD), which is used clinically in cardiovascular diseases has been recently reported to able to resist myocardial fibrosis. The anti-fibrosis effects of SMYAD have been evaluated; however, its intricate mechanisms remain to be clarified. Here, we found that SMYAD treatment reduced the fibrosis injury and collagen fiber deposition that could improve cardiac function in isoprenaline (ISO)-induced fibrosis rat models. Combined with our systematic RNA-seq data of SMYAD treatment, we demonstrated that the remarkable up-regulation or down-regulation of several genes were closely related to the functional enrichment of TGF-β and AMPK pathways that were involved in myocardial fibrosis. Accordingly, we further explored the molecular mechanisms of SMYAD were mainly caused by AMPK activation and thereby suppressing its downstream Akt/mTOR and TGF-β/SMAD3 pathways. Moreover, we showed that the ECM deposition and secretion process were attenuated, suggesting that the fibrosis pathological features are changed. Interestingly, we found the similar AMPK-driven pathways in NIH-3T3 mouse fibroblasts treated with ISO. Taken together, these results demonstrate that SMYAD may be a new candidate agent by regulating AMPK-driven Akt/mTOR and TGF-β/SMAD3 pathways for potential therapeutic implications of myocardial fibrosis.
Le texte complet de cet article est disponible en PDF.Abbreviations : SMYAD, ISO, ECM, EF%, FS%, LVESd, LVEDd, IVSd, LVPWd, EDV, ESV, HR, TGF-β
Keywords : Myocardial fibrosis, Traditional Chinese Medicine, Si-Miao-Yong-An Decoction, Extracellular matrix, AMPK
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Vol 130
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