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Updated: Mar 7, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Rg1-R1 attenuates cardiac ischemia/reperfusion-induced endothelial cell injury through activating the
Xiayinan Song1,2, Jinlan Deng1,2, Danyang Wang1,2
1Innovation Institute of Chinese Medicine and Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Background:
Mitochondrial dysfunction has been recognized as a pivotal pathological mechanism underlying myocardial ischemia/reperfusion injury (MIRI).Ginsenoside Rg1 and notoginsenoside R1 exhibits cardioprotective effects against MIRI. However, their molecular mechanisms remain unclear. This study aims to investigate the therapeutic potential of Rg1 and R1 in ameliorating cardiomyocyte injury through mitophagy regulation, with a focus on elucidating the molecular crosstalk between these compounds and key mitophagy-related signaling pathways.
Methods:
Cardiac injury in mice was induced by subjecting the heart to 45 min of ischemia followed by 6 h of reperfusion. Post-injury, the mice were treated with intraperitoneal injections of Rg1-R1. The effects of Rg1-R1 on MIRI were assessed through electrocardiography, echocardiography, HE/Masson staining, and Transmission Electron Microscope. The impact of Rg1-R1 on biochemical markers of myocardial injury was also analyzed. Cardiac microvascular endothelial cells (CMECs) were pretreated with Rg1-R1 prior to being exposed to hypoxia/reoxygenation (H/R). Subsequently, cellular function and mitochondrial function were evaluated.
Results:
Our results indicated that in vivo, Rg1-R1 improved MIRI-induced cardiac dysfunction; in vitro, exposure of CMECs to Rg1-R1 reduced H/R injury severity and protected mitochondria. Further studies illustrated the protective effect of Rg1-R1 achieved via the regulation of FUNDC1-mediated mitophagy. In addition, we found that Rg1-R1 exerted these protective effects by activating FUNDC1-dependent mitophagy through the ULK1/PGAM5 pathway.
Conclusions:
Our results indicated that Rg1-R1 attenuates MIRI-induced endothelial cell injury through activating the ULK1/PGAM5-FUNDC1-mitophagy pathway, and may represent a novel therapeutic target in the context of MIRI.
Insights
Ginsenoside Rg1 and R1 protect the heart from injury by activating mitophagy, a cellular cleanup process. These compounds target the ULK1/PGAM5-FUNDC1 pathway, offering a potential new treatment for myocardial ischemia/reperfusion injury.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Medicine
- Pharmacology
Background:
- Mitochondrial dysfunction is central to myocardial ischemia/reperfusion injury (MIRI).
- Ginsenoside Rg1 and notoginsenoside R1 (Rg1-R1) show cardioprotective effects, but their mechanisms are unclear.
- Understanding Rg1-R1's role in mitophagy is crucial for MIRI treatment.
Purpose of the Study:
- Investigate Rg1-R1's therapeutic potential in MIRI.
- Elucidate Rg1-R1's mechanism via mitophagy regulation.
- Explore the crosstalk between Rg1-R1 and mitophagy signaling pathways.
Main Methods:
- Induced MIRI in mice and treated with Rg1-R1.
- Assessed cardiac function using ECG, echocardiography, and histology.
- Evaluated Rg1-R1's effects on cardiac microvascular endothelial cells (CMECs) under hypoxia/reoxygenation (H/R).
Main Results:
- Rg1-R1 improved cardiac function and reduced MIRI in vivo.
- Rg1-R1 protected CMECs from H/R injury and preserved mitochondrial function in vitro.
- Rg1-R1 activated FUNDC1-mediated mitophagy via the ULK1/PGAM5 pathway.
Conclusions:
- Rg1-R1 attenuates MIRI-induced endothelial cell injury.
- The ULK1/PGAM5-FUNDC1-mitophagy pathway is key to Rg1-R1's protective effects.
- Rg1-R1 represents a potential novel therapeutic target for MIRI.
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