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Updated: Jan 11, 2026
Model of Ischemia and Reperfusion Injury in Rabbits
Published on: November 3, 2023
Novel Allogeneic Mitochondria and Associated Organelle Complex Treatment Prevents Myocardial Ischemia-Reperfusion
Takumi Hayashi1, Yuuki Shimizu1, Hisashi Ota2
1Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Background:
Ischemia-reperfusion (I/R) injury can damage mitochondria and lead to cardiomyocyte apoptosis. Freshly prepared autologous mitochondria have shown benefits against I/R injury, but it remains unclear whether allogeneic mitochondrial organelle complex Q (MRC-Q) after freeze-thawing can also be effective in this context.
Objectives:
This study aimed to determine whether administering MRC-Q can protect the heart from ischemia I/R injury in animal models.
Methods:
The MRC-Q used in our current experiments was intactly isolated by proprietary technology and cryopreserved. A mouse and porcine model of cardiac I/R injury was employed. In vitro experiments were performed using H9C2 cardiomyocytes subjected to hypoxic-reoxygenation conditions.
Results:
Our initial study demonstrated that MRC-Q can be storable with a maintenance of adenosine triphosphate production capacity. Next, we tested cardioprotective effects of MRC-Q administration on I/R injury in a murine model. Compared to the vehicle group, the MRC-Q-treated group showed a reduction in infarct size with fewer apoptotic cells, a decrease in circulating cardiac enzymes, and an improvement in cardiac function. In vitro studies revealed that MRC-Q was taken up into cardiomyocyte cells in a time-dependent manner. Next, we demonstrated that cell viability was improved in the MRC-Q-treated group after hypoxia/reoxygenation. Further examinations suggested that one of the mechanisms of cardioprotection by MRC-Q could be mediated by the secretion of mitochondria-derived peptides, which could inhibit apoptosis-promoting signals. In addition, MRC-Q augmented endogenous mitochondrial quality control in injured myocytes followed by up-regulation of adenosine triphosphate production and anti-reactive oxygen species activity. Finally, a preclinical pig model also confirmed the cardioprotective effects of MRC-Q administration.
Conclusions:
Our data demonstrated that freeze-thawed MRC-Q have a protective effect on the heart after I/R injury.
Insights
Freeze-thawed mitochondrial organelle complex Q (MRC-Q) effectively protects the heart from ischemia-reperfusion (I/R) injury. This cryopreserved therapy reduces heart damage, apoptosis, and improves cardiac function in animal models.
Area of Science:
- Cardiovascular Research
- Mitochondrial Biology
- Regenerative Medicine
Background:
- Ischemia-reperfusion (I/R) injury causes mitochondrial damage and cardiomyocyte apoptosis.
- Autologous mitochondria show promise, but allogeneic cryopreserved mitochondrial organelle complex Q (MRC-Q) efficacy is unexplored.
Purpose of the Study:
- To evaluate the cardioprotective potential of cryopreserved allogeneic MRC-Q against cardiac I/R injury in animal models.
Main Methods:
- Intact MRC-Q isolated and cryopreserved using proprietary technology.
- Cardiac I/R injury induced in mouse and preclinical pig models.
- In vitro studies using H9C2 cardiomyocytes under hypoxic-reoxygenation.
Main Results:
- Cryopreserved MRC-Q maintained adenosine triphosphate production capacity.
- MRC-Q treatment reduced infarct size, apoptosis, cardiac enzymes, and improved cardiac function in mice.
- In vitro, MRC-Q enhanced cardiomyocyte viability, upregulated ATP production, and antioxidant activity, potentially via secreted peptides.
Conclusions:
- Freeze-thawed MRC-Q demonstrates significant cardioprotective effects against I/R injury.
- Cryopreserved MRC-Q represents a viable therapeutic strategy for myocardial I/R injury.
