Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 130, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2020.110522
Keywords
Myocardial fibrosis; Traditional Chinese Medicine; Si-Miao-Yong-An Decoction; Extracellular matrix; AMPK
Funding
- National Natural Science Foundation of China [81603275]
- China Postdoctoral Science Foundation [2016M602697, 2018T110988]
- Open Fund of Key Laboratory of Ministry of Education for TCM VisceraState Theory and Applications, Liaoning University of Traditional Chinese Medicine [zyzx1910]
- Youth Project Funds from Department of Education of Liaoning Province [L201716]
- Doctoral Start-up Fund Program of Liaoning Province, China [20170520188]
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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-beta 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-beta/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-beta/SMAD3 pathways for potential therapeutic implications of myocardial fibrosis.
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