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Updated: Jan 20, 2026
Acute Myocardial Infarction in Rats
Published on: February 16, 2011
MiR-34a promotes myocardial infarction in rats by inhibiting the activity of SIRT1
1Department of Cardiology, Changhai Hospital, Shanghai, China. zhaoxx1112@126.com.
Objective:
To investigate the effect of micro ribonucleic acid (miR)-34a regulating silent information regulator 1 (SIRT1) on myocardial infarction (MI) rats.
Materials And Methods:
A total of 30 male, 8-week-old rats were divided into three groups, including: sham group (M group), MI group and MI + miR-34a treatment group (miR group). Tissue morphology in the MI region was observed via hematoxylin-eosin (HE) staining. Myocardial apoptosis in the three groups was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Furthermore, the protein levels of SIRT1, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in myocardial cells were detected via Western blotting.
Results:
Compared with M group, left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) increased significantly in MI group and miR group (p<0.05), while left ventricular ejection fraction (LVEF) and fractional shortening (FS) decreased obviously (p<0.05). The results of HE staining showed that the inflammatory infiltration of myocardial cells and intercellular collagen fibers significantly increased, and the neuronal damage was remarkably aggravated in MI group and miR group when compared with M group (p<0.05). Compared with MI group, myocardial necrosis, inflammatory cell infiltration and intercellular collagen fibers all increased significantly in miR group (p<0.05). Moreover, the results of TUNEL assay revealed that myocardial apoptosis rate in MI group [(21.35±3.12)%] was remarkably higher than that of M group [(9.53±1.17)%]. Meanwhile, it was significantly higher in miR group [(42.38±3.44)%)] than that of MI group, displaying statistically significant differences (p<0.05). The number of apoptotic cells increased obviously in MI group when compared with M group, while it decreased significantly in MI group when compared with miR group (p<0.05). Besides, the protein levels of SIRT1 and Bcl-2 in myocardial tissues in miR group were remarkably lower than those of M group and MI group (p<0.05). Furthermore, the protein level of Bax in miR group was higher than that of M group and MI group, and there were statistically significant differences (p<0.05).
Conclusions:
Overexpression of miR-34a inhibits the activity of SIRT1, thereby promoting the apoptosis of MI.
Insights
Overexpression of microRNA-34a (miR-34a) exacerbates myocardial infarction (MI) in rats by inhibiting silent information regulator 1 (SIRT1), leading to increased apoptosis and worsened cardiac function.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Myocardial infarction (MI) is a leading cause of heart failure.
- MicroRNAs (miRNAs) play crucial roles in cardiac pathophysiology.
- The specific role of miR-34a in MI progression warrants further investigation.
Purpose of the Study:
- To investigate the effect of microRNA-34a (miR-34a) on myocardial infarction (MI) in a rat model.
- To elucidate the regulatory relationship between miR-34a and silent information regulator 1 (SIRT1) in the context of MI.
- To assess the impact of miR-34a on myocardial apoptosis and cardiac function.
Main Methods:
- Establishment of a rat model of myocardial infarction.
- Grouping of rats into sham, MI, and MI + miR-34a treatment groups.
- Assessment of cardiac function using echocardiography (LVEDD, LVESD, LVEF, FS).
- Histopathological analysis (HE staining) for tissue morphology and inflammation.
- Detection of myocardial apoptosis via TUNEL assay.
- Quantification of protein levels (SIRT1, Bcl-2, Bax) using Western blotting.
Main Results:
- MI and miR-34a treatment significantly increased cardiac dimensions (LVEDD, LVESD) and decreased cardiac function (LVEF, FS).
- Histology revealed aggravated myocardial damage, inflammation, and collagen deposition in MI and miR-34a treated groups compared to sham.
- miR-34a treatment further worsened myocardial necrosis, inflammation, and collagen fibrosis compared to the MI group.
- Myocardial apoptosis rate was significantly higher in the MI group and further elevated in the miR-34a treated group.
- Overexpression of miR-34a led to decreased protein levels of SIRT1 and Bcl-2, and increased Bax protein levels.
Conclusions:
- Overexpression of miR-34a exacerbates myocardial infarction in rats.
- miR-34a inhibits the activity of SIRT1, a key regulator in cardiac protection.
- The miR-34a/SIRT1 axis promotes myocardial apoptosis and worsens cardiac dysfunction post-MI.
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