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Updated: Jun 21, 2026
Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
c-Jun DNAzymes inhibit myocardial inflammation, ROS generation, infarct size, and improve cardiac function after
1Centre for Vascular Research, University of New South Wales, Sydney, NSW, Australia.
Insights
Catalytic DNA (DNAzymes) targeting c-Jun reduce heart attack infarct size by inhibiting inflammation and cell death. This novel therapy, Dz13, improves cardiac function after ischemia-reperfusion injury.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Inflammation Research
Background:
- Coronary reperfusion is standard for reducing infarct size post-heart attack.
- Reperfusion paradoxically causes myocardial injury via inflammation, necessitating new treatments.
Purpose of the Study:
- To investigate the role of c-Jun in myocardial ischemia-reperfusion injury.
- To evaluate the therapeutic potential of DNAzymes targeting c-Jun (Dz13) in reducing infarct size and improving cardiac function.
Main Methods:
- Assessed c-Jun expression post-myocardial ischemia-reperfusion injury.
- Administered synthetic catalytic DNA molecules (DNAzymes) targeting c-Jun (Dz13) intramyocardially at ischemia or reperfusion.
- Evaluated infarct size, inflammatory cell infiltration (neutrophils, C3, C3aR, Mac-1), apoptosis, reactive oxygen species, and cardiac function.
Main Results:
- c-Jun expression is induced after myocardial ischemia-reperfusion injury.
- Dz13 treatment significantly reduced infarct size in the area-at-risk (AAR).
- Dz13 attenuated neutrophil infiltration, c-Jun and ICAM-1 expression, cardiomyocyte apoptosis, and reactive oxygen species generation. It also inhibited inflammatory cell infiltration (C3, C3aR, Mac-1, MMP-2) and improved cardiac function without affecting vascularity or fibrosis.
Conclusions:
- c-Jun plays a key regulatory role in myocardial inflammation and infarction following ischemia-reperfusion injury.
- Catalytic DNA (Dz13) effectively inhibits c-Jun-mediated pathways, offering a promising therapeutic strategy for myocardial ischemia-reperfusion injury.
Objective:
Coronary reperfusion has been the mainstay therapy for reduced infarct size after a heart attack. However, this intervention also results in myocardial injury by initiating a marked inflammatory reaction, and new treatments are keenly sought.
Methods And Results:
The basic-region leucine zipper protein, c-Jun is poorly expressed in the normal myocardium and is induced within 24 hours after myocardial ischemia-reperfusion injury. Synthetic catalytic DNA molecules (DNAzymes) targeting c-Jun (Dz13) reduce infarct size in the area-at-risk (AAR) regardless of whether it is delivered intramyocardially at the initiation of ischemia or at the time of reperfusion. Dz13 attenuates neutrophil infiltration, c-Jun and ICAM-1 expression in vascular endothelium, cardiomyocyte apoptosis, and the generation of reactive oxygen species in the reperfused myocardium. It inhibits infiltration into the AAR of complement 3 (C3), C3a receptor (C3aR), membrane attack complex-1 (Mac-1), or matrix metalloproteinase-2 (MMP-2) positive inflammatory cells. Dz13 also improves cardiac function without influencing myocardial vascularity or fibrosis.
Conclusions:
These findings demonstrate the regulatory role of c-Jun in the pathogenesis of myocardial inflammation and infarction following ischemia-reperfusion injury, and inhibition of this process using catalytic DNA.
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