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Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Protective Effect of Polydeoxyribonucleotide Against Renal Ischemia-Reperfusion Injury in Mice
E K Jeong1, H J Jang2, S S Kim1
1Department of Anesthesia and Pain Medicine, Ulsan University College of Medicine, Gangneung Asan Hospital, Gangneung, South Korea.
Background:
Polydeoxyribonucleotide (PDRN) is an A2A receptor agonist that induces vascular endothelial growth factor (VEGF) production during the pathological condition of low tissue perfusion. Ischemia-reperfusion injury (IRI) is a major problem after renal transplantation. In the present study, we investigated whether PDRN exhibits reno-protective effects against ischemia-reperfusion-induced acute kidney injury in mice.
Methods:
Renal ischemia-reperfusion injury was induced in male C57BL/6 mice by bilateral renal pedicle occlusion for 30 minutes, followed by reperfusion for 48 hours. PDRN (8 mg/kg body weight intraperitoneally) was administered 30 minutes before IRI.
Results:
Treatment with PDRN significantly decreased neutrophil gelatinase-associated lipocalin levels in the urine, blood urea nitrogen level, and serum creatinine levels as well as kidney tubular injury. Western blotting showed that PDRN significantly increased the levels of vascular endothelial growth factor and B-cell lymphoma protein and attenuated p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, inducible nitric oxide synthase, and Bcl-2-associated X protein levels 48 hours after IRI.
Conclusions:
Our findings suggest that PDRN is a potential therapeutic agent for acute ischemia-induced renal damage.
Insights
Polydeoxyribonucleotide (PDRN) shows promise in protecting kidneys from ischemia-reperfusion injury (IRI). This study found PDRN reduced kidney damage markers and inflammation in mice, suggesting its therapeutic potential for acute renal injury.
Area of Science:
- Nephrology
- Transplantation Immunology
- Pharmacology
Background:
- Polydeoxyribonucleotide (PDRN) acts as an A2A receptor agonist, stimulating vascular endothelial growth factor (VEGF) production in low tissue perfusion states.
- Ischemia-reperfusion injury (IRI) poses a significant challenge in renal transplantation, leading to acute kidney injury.
- The study explores PDRN's potential renoprotective effects against IRI-induced acute kidney injury in a murine model.
Purpose of the Study:
- To investigate the renoprotective efficacy of PDRN against ischemia-reperfusion-induced acute kidney injury.
- To evaluate PDRN's impact on key biomarkers and cellular pathways involved in renal IRI.
Main Methods:
- Male C57BL/6 mice underwent bilateral renal pedicle occlusion for 30 minutes, followed by 48 hours of reperfusion to induce IRI.
- PDRN (8 mg/kg body weight) was administered intraperitoneally 30 minutes prior to the induction of IRI.
Main Results:
- PDRN treatment significantly reduced urinary neutrophil gelatinase-associated lipocalin, blood urea nitrogen, and serum creatinine levels.
- Histological analysis revealed decreased kidney tubular injury in PDRN-treated mice.
- Western blotting demonstrated increased VEGF and Bcl-2 levels, alongside attenuated p38 MAPK, JNK, iNOS, and Bax expression post-IRI.
Conclusions:
- PDRN exhibits significant renoprotective effects against IRI-induced acute kidney injury.
- PDRN may serve as a valuable therapeutic agent for mitigating renal damage caused by ischemia.
- The observed molecular changes suggest PDRN modulates inflammatory and apoptotic pathways relevant to renal IRI.

