Transplantation proceedings · 2026
The Therapeutic Effect of Polydeoxyribonucleotide on Lung Ischemia-Reperfusion Injury.
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Sun Fenghua, Xu Cong
Аннотация
OBJECTIVE: This study aims to explore the therapeutic role of polydeoxyribonucleotide (PDRN) in lung ischemia-reperfusion injury (LIRI).
METHODS: A mouse model of LIRI was established. Experimental groups included the control group, model group, model + low-dose PDRN group, model + high-dose PDRN group, and model + high-dose PDRN combined with AKT inhibitor group. Pathological changes in mouse lung tissues were observed using H&E staining, and cell apoptosis was detected via TUNEL assay. Serum levels of malondialdehyde (MDA) and interleukin-1β (IL-1β) were measured, while protein expression levels of BCL-2, BAX, cleaved-Caspase-3, and p-AKT/AKT were determined using Western blot.
RESULTS: Compared with the control group, the model group showed bronchial wall thickening in lung tissues, with extensive red blood cell infiltration and inflammatory cell accumulation in the lung interstitium, indicating significant tissue damage. Additionally, levels of IL-1β, MDA, BAX, and cleaved-Caspase-3 were elevated, while BCL-2 expression and p-AKT/AKT ratio were reduced. In contrast, the model + low-dose PDRN group and model + high-dose PDRN group exhibited alleviated lung tissue damage, reduced inflammatory cell infiltration, decreased levels of IL-1β, MDA, BAX, and cleaved-Caspase-3, and increased BCL-2 expression and p-AKT/AKT ratio, suggesting therapeutic effects. However, in the model + high-dose PDRN + AKT inhibitor group, lung tissue damage, inflammatory responses, and cell apoptosis were aggravated, with increased IL-1β, MDA, BAX, and cleaved-Caspase-3 levels, and decreased BCL-2 expression and p-AKT/AKT ratio.
CONCLUSIONS: PDRN exerts a therapeutic effect on LIRI by reducing cell apoptosis and inflammatory responses through the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway.
METHODS: A mouse model of LIRI was established. Experimental groups included the control group, model group, model + low-dose PDRN group, model + high-dose PDRN group, and model + high-dose PDRN combined with AKT inhibitor group. Pathological changes in mouse lung tissues were observed using H&E staining, and cell apoptosis was detected via TUNEL assay. Serum levels of malondialdehyde (MDA) and interleukin-1β (IL-1β) were measured, while protein expression levels of BCL-2, BAX, cleaved-Caspase-3, and p-AKT/AKT were determined using Western blot.
RESULTS: Compared with the control group, the model group showed bronchial wall thickening in lung tissues, with extensive red blood cell infiltration and inflammatory cell accumulation in the lung interstitium, indicating significant tissue damage. Additionally, levels of IL-1β, MDA, BAX, and cleaved-Caspase-3 were elevated, while BCL-2 expression and p-AKT/AKT ratio were reduced. In contrast, the model + low-dose PDRN group and model + high-dose PDRN group exhibited alleviated lung tissue damage, reduced inflammatory cell infiltration, decreased levels of IL-1β, MDA, BAX, and cleaved-Caspase-3, and increased BCL-2 expression and p-AKT/AKT ratio, suggesting therapeutic effects. However, in the model + high-dose PDRN + AKT inhibitor group, lung tissue damage, inflammatory responses, and cell apoptosis were aggravated, with increased IL-1β, MDA, BAX, and cleaved-Caspase-3 levels, and decreased BCL-2 expression and p-AKT/AKT ratio.
CONCLUSIONS: PDRN exerts a therapeutic effect on LIRI by reducing cell apoptosis and inflammatory responses through the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway.