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Qishen capsule safely boosts cardiac function and angiogenesis via the MEK/ERK pathway in a rat myocardial infarction model

BACKGROUND: Qishen (QS) capsules, a Traditional Chinese Medicine, has been widely used to treat coronary heart disease in China. However, evidence of its effectiveness remains unclear. METHODS: To explore whether QS has cardioprotective efficacy and/or promotes angiogenesis after myocardial infarcti...

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Detalles Bibliográficos
Autores principales: Guo, Cai-Xia, Li, Zhi-Yuan, Niu, Jin-Bang, Fan, Shuan-Cheng, Yan, Si-Yu, Lu, Pei-Pei, Su, Yan-Ni, Ma, Li-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Science Press 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6828606/
https://www.ncbi.nlm.nih.gov/pubmed/31700516
http://dx.doi.org/10.11909/j.issn.1671-5411.2019.10.008
Descripción
Sumario:BACKGROUND: Qishen (QS) capsules, a Traditional Chinese Medicine, has been widely used to treat coronary heart disease in China. However, evidence of its effectiveness remains unclear. METHODS: To explore whether QS has cardioprotective efficacy and/or promotes angiogenesis after myocardial infarction (MI), we performed experiments in a preclinical rat MI model. One month after left anterior descending coronary artery ligation, the rats received either QS solution (0.4 g/kg/day) or the same volume of saline by intragastric injection for four weeks. RESULTS: Echocardiographic and hemodynamic analyses demonstrated relatively preserved cardiac function in MI rats administered QS. Indeed, QS treatment was associated with reduced infarct scar size and heart weight index, and these beneficial effects were responsible for enhancing angiogenesis. Mechanistically, QS treatment increased phosphorylation of protein kinase B (Akt) and downregulated phosphorylation of mitogen-activated protein kinase/extracellular-regulated kinase (MEK/ERK). CONCLUSIONS: QS therapy can improve the cardiac function of rats after MI by an underlying mechanism involving increased angiogenesis, at least partially via activation of the Akt signaling pathway and inhibition of MEK/ERK phosphorylation.