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Updated: Mar 21, 2026
A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
Post-conditioning anti-PUMA treatment protects mice against mice heart I/R injury
1Department of Anesthesia, the Affiliated Hospital of Qingdao University, Qingdao, Shandong, China. chuhaichenqd@126.com.
Objective:
PUMA is a pro-apoptotic gene, which has been found to be critical to the pathogenesis during heart ischemia-reperfusion injury (IRI). We investigate whether anti-PUMA protect mice from acute heart failure.
Materials And Methods:
Mice were subjected to 30 min ischemia and 24 hrs reperfusion in the presence or absence of anti-PUMA. Treated mice were evaluated for heart PUMA protein and mRNA expression, and apoptosis by terminal deoxy nucleotidyltransferase-mediated dUTP nick end labeling (TUNEL) staining.
Results:
In mice, anti-PUMA post conditioning markedly reduced PUMA mRNA and protein expression in the heart 4-fold. Hearts from mice that received anti-PUMA had substantially fewer heart muscles apoptosis by TUNEL staining. Anti-PUMA post-conditioning greatly reduced infarct size to 14.4±3.7%, from 38.2±3.9% in the untreated I/R group. Furthermore, survival experiments revealed that more than 90% of control mice died from lethal I/R, whereas 20% of the anti-PUMA post-treated mice survived until the end of the 10-day observation period.
Conclusions:
This study confirms the importance of PUMA-mediated apoptosis in heart ischemia-reperfusion injury. Silencing PUMA by recombinant PUMA has therapeutic promise to limit ischemia-reperfusion injury.
Insights
Targeting the pro-apoptotic gene PUMA with anti-PUMA therapy significantly protects mice from acute heart failure following ischemia-reperfusion injury. This approach reduces heart muscle apoptosis and infarct size, improving survival rates.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cell Death Pathways
Background:
- PUMA is a pro-apoptotic gene crucial in heart ischemia-reperfusion injury (IRI).
- Acute heart failure is a significant complication of IRI.
Purpose of the Study:
- To investigate the protective effects of anti-PUMA therapy against acute heart failure induced by IRI in mice.
- To evaluate the impact of PUMA inhibition on cardiac apoptosis and infarct size.
Main Methods:
- Mice underwent 30 minutes of ischemia followed by 24 hours of reperfusion, with or without anti-PUMA treatment.
- Cardiac PUMA expression (mRNA and protein) and apoptosis (TUNEL staining) were assessed.
- Infarct size and survival rates were determined.
Main Results:
- Anti-PUMA post-conditioning reduced cardiac PUMA expression by 4-fold.
- Apoptosis and infarct size were substantially decreased in anti-PUMA treated mice compared to controls.
- Survival rates improved significantly, with 20% of treated mice surviving versus <10% in the control group.
Conclusions:
- PUMA-mediated apoptosis plays a critical role in IRI pathogenesis.
- Silencing PUMA using recombinant anti-PUMA demonstrates therapeutic potential for limiting IRI and acute heart failure.
