Abstract
Lung injury is characterized by diffuse lung inflammation, alveolar-capillary destruction, and alveolar flooding, resulting in respiratory failure. Polydexyribonucleotide (PDRN) has an anti-inflammatory effect, decreasing inflammatory cytokines, and suppressing apoptosis. Thus, we investigated its efficacy in the treatment of lung injury, which was induced in rats using lipopolysaccharide (LPS). Rats were randomly divided into three groups according to sacrifice time, and each group split into control, lung injury-induced, and lung injury-induced + PDRN-treated groups. Rats were sacrificed 24 h and 72 h after PDRN administration, according to each group. Lung injury was induced by intratracheal instillation of LPS (5 mg/kg) in 0.2 mL saline. Rats in PDRN-treated groups received a single intraperitoneal injection of 0.3 mL distilled water including PDRN (8 mg/kg), 1 h after lung injury induction. Percentages of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive, cleaved caspase-3-, -8-, and -9-positive cells, the ratio of Bcl-2-associated X protein (Bax) to B-cell lymphoma 2 (Bcl-2), and expressions of inflammatory cytokines (tumor necrosis factor-α, interleukin-6) were decreased by PDRN treatment in the LPS-induced lung injury rats. Therefore, treatment with PDRN reduced lung injury score. This anti-apoptotic effect of PDRN can be ascribed to the enhancing effect of PDRN on adenosine A2A receptor expression. Based on these results, PDRN might be considered as a new therapeutic agent for the treatment of lung injury.
Highlights
Acute lung injury (ALI) is characterized by disruption of the alveolar-capillary membrane barrier and resultant pulmonary edema, and is associated with proteinaceous alveolar exudate [1]
We investigated the effect of PDRN treatment on lipopolysaccharide (LPS)-induced lung injury using rats
These results indicate that cleaved caspase-3, -8, and -9 expressions were significantly increased by the induction of lung injury (p < 0.05), whereas, PDRN treatment significantly decreased cleaved
Summary
Acute lung injury (ALI) is characterized by disruption of the alveolar-capillary membrane barrier and resultant pulmonary edema, and is associated with proteinaceous alveolar exudate [1]. Apoptosis is a ‘clean’ form of cell death, apoptotic cells that are not rapidly removed eventually undergo secondary necrosis associated with leakage of cellular content and inflammation, leading to severe tissue damage [10]. Caspases are a family of proteases that play an essential role in programmed cell death and inflammation. The cleaved forms of caspases activate pro-apoptotic pathways leading to DNA degradation and cell death [13]. B-cell lymphoma 2 (Bcl-2) family proteins play an important role in the regulation of apoptosis. The imbalance between pro-apoptotic and anti-apoptotic mediators causes apoptosis and increases susceptibility to lung injury [15]. PDRN is known to promote wound healing and suppress apoptotic cell death, the effects of PDRN on lung injury have not been reported. TUNEL assay, immunohistochemistry for cleaved caspase-3, -8, -9, and Western blotting for Bax, Bcl-2, TNF-α, IL-6, and adenosine A2A receptors were performed
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