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Updated: May 12, 2026
A Modified Simple Method for Induction of Myocardial Infarction in Mice
Published on: December 3, 2021
Cyanidin prevents cardiomyocyte apoptosis in mice after myocardial infarction
Deng Gang1,2,3, Ouyang Qing1,2,4, Yongzheng Yang2,3,4
1School of Medicine, South China University of Technology, Guangzhou, 510006, People's Republic of China.
Insights
Cyanidin, a natural flavonoid, was studied for its effects on myocardial infarction in mice. It was found to improve cardiac function, reduce cell death, and mitigate tissue damage by inhibiting specific enzymes and pathways.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Natural Product Chemistry
Background:
- Myocardial infarction (MI) is a leading cause of heart failure globally.
- Natural compounds, like flavonoids, show potential in cardiovascular disease treatment.
- Anthocyanidins possess antioxidant and anti-inflammatory properties beneficial for heart health.
Purpose of the Study:
- To investigate the cardioprotective effects of cyanidin in a mouse model of myocardial infarction.
- To elucidate the molecular mechanisms underlying cyanidin's therapeutic actions.
Main Methods:
- Myocardial infarction was induced in C57BL/6 mice.
- Cyanidin was administered orally for four weeks.
- Cardiac function, gene expression (RNAseq, Western blot), histology (Masson, HE, TEM), apoptosis (TUNEL), and serum biomarkers (BNP, ANP via ELISA) were assessed.
- Molecular docking simulations were performed.
Main Results:
- Cyanidin treatment improved cardiac function and reduced myocardial apoptosis and histological damage.
- Serum levels of B-type natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) were decreased.
- Cyanidin inhibited matrix metalloproteinases (MMP2/9) and Fibronectin 1 (Fn1) activity.
- Inhibition of MMP9/2 and modulation of the Akt signaling pathway were suggested mechanisms.
Conclusions:
- Cyanidin demonstrates significant cardioprotective effects against myocardial infarction in mice.
- It prevents cardiomyocyte apoptosis and improves cardiac function.
- The therapeutic benefits are likely mediated through the suppression of MMPs and regulation of the Akt pathway, identifying potential therapeutic targets.
Abstract:
Myocardial infarction is a worldwide disease with high morbidity and mortality and a major cause of chronic heart failure, seriously affecting patients' quality of life. Natural medicine has been used to cure or prevent cardiovascular disease for decades. As a natural flavonoid, anthocyanidin has been used to treat many diseases due to its antioxidative, anti-inflammatory, and other properties. A mouse model (C57BL/6) weighing 30-40 g was utilized to induce myocardial infarction by ligating the left anterior descending coronary artery. Cyanidin (30 mg/kg) was administered orally to mice for four weeks. A variety of assessments were used to evaluate cardiac function. The gene expression was measured using RNAseq and Western blot. Histological changes in myocardial tissue were assessed using staining techniques, including Masson, Hematoxylin Eosin (HE), and transmission electron microscopy. Tunnel staining was implemented as a method to detect cellular apoptosis. For the quantification of B-type natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) in the serum, an enzyme-linked immunosorbent assay (ELISA) was employed. Furthermore, autodock simulation was executed in order to assess the interaction between cyanidin and a subset of genes. Cyanidin treatment inhibited myocardial cell apoptosis, improved cardiac function, and reduced serum concentrations of BNP and atrial natriuretic peptide ANP, as well as mitigated histological cardiac tissue damage. Cyanidin also inhibited the activity of matrix metalloproteinases (MMP2/9) and Fibronectin 1 (Fn1). Cyanidin improves heart function and reduces myocardial damage in mice after MI. Furthermore, cyanidin can prevent cardiomyocyte apoptosis. These effects are most likely caused by suppression of MMP9/2 and control of the Akt signaling pathway, suggesting an appropriate therapeutic target.
