Key result
QSYQ ameliorated cardiac fibrosis and attenuated cardiomyocyte apoptosis after pressure overload-induced cardiac hypertrophy by regulating FHL2 and the macrophage RP S19/TGF-β1 signaling pathway.
Why the study?
Effective treatments to block cardiac fibrosis after cardiac hypertrophy are lacking, and the mechanisms underlying QiShenYiQi pill's efficacy in chronic heart failure remain unclear.
Does QiShenYiQi pill reduce cardiac fibrosis and myocardial apoptosis in a rat model of pressure overload-induced cardiac hypertrophy?
Population
Rats with pressure overload-induced cardiac hypertrophy and H9C2, Raw264.7, and RDF cell models
Comparison
QiShenYiQi pill administration
Design
In vivo animal model and in vitro cell study
Follow-up
6 weeks
Authors
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Hypothesis-generating for QSYQ in rat hypertrophy; clinical trials needed before human use.
Does QiShenYiQi pill reduce cardiac fibrosis and myocardial apoptosis in a rat model of pressure overload-induced cardiac hypertrophy?
p-value: p=<0.05
The QiShenYiQi pill ameliorates cardiac fibrosis and apoptosis in a rat model of pressure overload-induced hypertrophy by regulating FHL2 and the macrophage RP S19/TGF-β1 signaling pathway.
Anwaier et al. (2022) studied Pressure overload-induced cardiac hypertrophy and fibrosis. QiShenYiQi Pill (QSYQ) vs. Vehicle/Sham or Trimetazidine (TMZ) was evaluated on Cardiac fibrosis and myocardial apoptosis (p=<0.05). QSYQ ameliorated cardiac fibrosis and attenuated cardiomyocyte apoptosis after pressure overload-induced cardiac hypertrophy by regulating FHL2 and the macrophage RP S19/TGF-β1 signaling pathway.
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