ArticlePloS one2024
Qili Qiangxin capsule attenuates myocardial fibrosis by modulating collagen homeostasis post-infarction in rats.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Qiliqiangxin capsule attenuates platelet activation and thrombosis by suppressing CaThrombosis journal · 2026Article
- Research progress on targeting autophagy pathways with medicinal plants and their active metabolites for the treatment of heart failure.Frontiers in pharmacology · 2026Review
- The effectiveness and safety of oral Chinese patent medicines in treating myocardial infarction complicated with heart failure: a network meta-analysis of 12 interventions.Frontiers in cardiovascular medicine · 2026Review
- Chinese and western medicine treatment of myocardial fibrosis drugs.Frontiers in cardiovascular medicine · 2024Review
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7 authors.
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Abstract
Myocardial fibrosis (MF) is a major cause of morbidity and mortality worldwide. Qili Qiangxin capsule (QLQX) is a traditional Chinese medicine (TCM) formula used for treating MF, QLQX can affect ventricular remodeling by regulating collagen deposition; however, the specific mechanism by which QLQX modulates collagen homeostasis remains unclear. Thus, this study aimed to explore the effect of QLQX on collagen fibers and its mechanism of action in rats after myocardial infarction (MI). Rats were subjected to left anterior descending artery ligation and then were divided equally into five groups: sham, model, low-dose QLQX, high-dose QLQX and empagliflozin groups. QLQX treatment for 28 days significantly improved cardiac function, as evidenced by decreases in heart mass index, cardiac volume, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, N-terminal B-type natriuretic peptide levels, and high-sensitivity cardiac troponin I levels and increases in left ventricular ejection fraction and left ventricular fraction shortening. Hematoxylin and eosin, Masson, and Picrosirius red staining under a light microscope indicated that QLQX treatment suppressed fibrosis and promoted angiogenesis by decreasing the protein expression levels of proteins related to cardiac remodeling including transforming growth factor-β1, metalloproteinase-9 and α-smooth muscle actin and increasing the expression of tissue inhibitor of matrix metalloproteinase-1 concentration. Picrosirius red staining under the polarized light microscope and western blotting showed that MI increased the contents of collagen I and III, and reduced the contents of collagen II and IV. QLQX treatment improved cardiac function and attenuated MF by modulating collagen homeostasis and promoting angiogenesis. This study provides novel insights into the mechanism of action of QLQX in preventing MF after MI.
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