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January 20, 2022Open Access

Network pharmacology exploration reveals the bioactive compounds and molecular mechanisms by which Gui-Qi-Yang-Xin Decoction suppresses myocardial fibrosis

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Key result

Gui-Qi-Yang-Xin Decoction alleviates isoproterenol-induced myocardial fibrosis in rats and cells by modulating PTGS2, MAPK, and AKT1.

  • n=90

Why the study?

Gui-Qi-Yang-Xin Decoction exerts therapeutic effects on myocardial fibrosis, but its bioactive compounds and underlying pharmacological mechanisms remain to be elucidated.

Population

Isoproterenol-induced myocardial fibrosis rats and H9C2 cells

Comparison

Gui-Qi-Yang-Xin Decoction vs controls

Design

Network pharmacology study with in vivo animal and in vitro cell experimental validation

Authors

HJHugang JiangWLWenyan LinXWXinqiang Wang

Discussion

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Overview

Supports preclinical exploration of GQYXD in myocardial fibrosis; leaves open clinical translation in humans.

Structured PICO

P
Population
90 male Wistar rats and H9C2 rat cardiomyoblast cells used to model isoproterenol-induced myocardial fibrosis.
I
Intervention
Gui-Qi-Yang-Xin Decoction (GQYXD)
O
Outcome
Alleviation of myocardial fibrosis and organizational damage to cell cytoskeletonsurrogate

Gui-Qi-Yang-Xin Decoction alleviates myocardial fibrosis in preclinical models via modulation of PTGS2, MAPK14, MAPK8, and AKT1 pathways.

Limitations

  • Further animal experimental research is needed to fully explain the therapeutic mechanisms of TCM.

Cite This Study

Jiang et al. (2022) studied Myocardial fibrosis (n=90). Gui-Qi-Yang-Xin Decoction (GQYXD) vs. Isoproterenol-induced model group was evaluated on Myocardial fibrosis alleviation and regulation of PTGS2, MAPK14, AKT1, and MAPK8 expression. Gui-Qi-Yang-Xin Decoction alleviated isoproterenol-induced myocardial fibrosis in rats and H9C2 cells by down-regulating PTGS2, MAPK14, and MAPK8, and up-regulating AKT1 expression.

synapsesocial.com/papers/6aa8c655badca0387dda7733https://doi.org/10.21203/rs.3.rs-1263524/v1
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