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Updated: Dec 22, 2025
Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
MiR-129-5p protects against myocardial ischemia-reperfusion injury via targeting HMGB1
1Department of Laboratory Medicine, Houjie Hospital of Dongguan, Dongguan, P.R. China. 332689892@qq.com.
Objective:
To investigate the protective effect of miR-129-5p on ischemia-reperfusion (I/R) injury via targeting high mobility group box-1 (HMGB1).
Materials And Methods:
Rat models of myocardial I/R and hypoxia/reoxygenation (H/R) cardiomyocytes were established, and the miR-129-5p and HMGB1 expression levels in myocardium of I/R rats and in cardiomyocytes of H/R rats were quantified by RT-PCR. The over-expression of miR-129-5p was performed on I/R rats, and the over-expression of miR-129-5p and down-regulation of HMGB1 were performed on cardiomyocytes of H/R rats. Triphenyltetrazolium chloride (TTC) staining was used to measure myocardial infarct size (IS). TUNEL (TdT-mediated dUTP end nick labeling) staining was employed to observe cardiomyocyte apoptosis in the myocardium of rats, and flow cytometry to observe cardiomyocyte apoptosis of I/R and H/R rats respectively. Dual-Luciferase reporter assay was used to verify the target relation between miR-129-5p and HMGB1.
Results:
MiR-129-5p was lowly expressed and HMGB1 was highly expressed in myocardial I/R injury rats and cardiomyocytes of H/R rats. Over-expression of miR-129-5p effectively reduced myocardial IS and cardiomyocyte apoptosis in rats with myocardial I/R injury, and significantly down-regulated the pro-apoptotic protein Bax, as well as significantly up-regulated the anti-apoptotic protein Bcl-2. Either over-expression of miR-129-5p or low-expression of HMGB1 in cardiomyocytes of H/R rats also achieved the same effects as described above. Dual-Luciferase reporter assay determined that miR-129-5p was a target for HMGB1.
Conclusions:
MiR-129-5p plays a protective role on myocardial I/R injury by regulating HMGB1 expression. Besides, it inhibits cardiomyocyte apoptosis and is expected to become a novel molecular marker or therapeutic target for myocardial I/R injury.
Insights
MicroRNA-129-5p protects against myocardial ischemia-reperfusion (I/R) injury by targeting high mobility group box-1 (HMGB1). Upregulating miR-129-5p reduces heart cell apoptosis and infarct size, offering a potential therapeutic target.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genetics and Genomics
Background:
- Myocardial ischemia-reperfusion (I/R) injury is a significant clinical concern.
- Understanding the molecular mechanisms underlying I/R injury is crucial for developing effective treatments.
- MicroRNAs (miRNAs) have emerged as key regulators in cardiovascular diseases.
Purpose of the Study:
- To investigate the protective role of microRNA-129-5p (miR-129-5p) in myocardial I/R injury.
- To elucidate the underlying molecular mechanism involving high mobility group box-1 (HMGB1).
- To assess the potential of miR-129-5p as a therapeutic target for I/R injury.
Main Methods:
- Establishment of rat models for myocardial I/R and hypoxia/reoxygenation (H/R) in cardiomyocytes.
- Quantification of miR-129-5p and HMGB1 expression using RT-PCR.
- Overexpression of miR-129-5p and HMGB1 manipulation in experimental models.
- Assessment of myocardial infarct size (IS) via TTC staining and cardiomyocyte apoptosis using TUNEL staining and flow cytometry.
- Verification of the targeting relationship between miR-129-5p and HMGB1 using Dual-Luciferase reporter assay.
Main Results:
- MiR-129-5p expression was found to be downregulated, while HMGB1 expression was upregulated in myocardial I/R injury.
- Overexpression of miR-129-5p significantly reduced myocardial IS and cardiomyocyte apoptosis.
- miR-129-5p modulated the expression of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins.
- Dual-Luciferase reporter assay confirmed HMGB1 as a direct target of miR-129-5p.
Conclusions:
- MiR-129-5p exerts a protective effect against myocardial I/R injury by regulating HMGB1 expression.
- MiR-129-5p inhibits cardiomyocyte apoptosis, suggesting its potential as a novel molecular marker.
- This study highlights miR-129-5p as a promising therapeutic target for myocardial I/R injury.
