[논문]Polydeoxyribonucleotide ameliorates lipopolysaccharide-induced acute lung injury via modulation of the MAPK/NF-κB signaling pathway in rats

Ko, Il-Gyu; Hwang, Jae Joon; Chang, Bok Soon; Kim, Sang-Hoon; Jin, Jun-Jang; Hwang, Lakkyong; Kim, Chang-Ju; Choi, Cheon Woong

doi:10.1016/j.intimp.2020.106444

Polydeoxyribonucleotide ameliorates lipopolysaccharide-induced acute lung injury via modulation of the MAPK/NF-κB signaling pathway in rats

International immunopharmacology, v.83, 2020년, pp.106444 -

Ko, Il-Gyu (Department of Physiology, College of Medicine, Kyung Hee University) , Hwang, Jae Joon (Department of Pulmonary and Critical Care Medicine, Kyung Hee University Hospital at Gangdong) , Chang, Bok Soon (Department of Pulmonary and Critical Care Medicine, Kyung Hee University Hospital at Gangdong) , Kim, Sang-Hoon (Department of Physiology, College of Medicine, Kyung Hee University) , Jin, Jun-Jang (Department of Physiology, College of Medicine, Kyung Hee University) , Hwang, Lakkyong (Department of Physiology, College of Medicine, Kyung Hee University) , Kim, Chang-Ju (Department of Physiology, College of Medicine, Kyung Hee University) , Choi, Cheon Woong (Department of Pulmonary and Critical Care Medicine, Kyung Hee University Hospital at Gangdong)

Abstract ▼ AI-Helper

Abstract Acute lung injury (ALI) is characterized by disruption of the alveolar-capillary membrane resulting in pulmonary edema and accumulation of associated proteinaceous alveolar exudate. Initiation of ALI upregulates tumor necrosis factor-α (TNF-α), which activates nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPK) that induce various pro-inflammatory mediators. Polydexyribonucleotide (PDRN) is an adenosine A2A receptor agonist that exerts anti-inflammatory effects by suppressing the production of pro-inflammatory cytokines and apoptosis. We investigated the therapeutic efficiency of PDRN on ALI induced by lipopolysaccharide (LPS) in rats. ALI was induced by intratracheal instillation of LPS (5 mg/kg) in 200 μL saline. The PDRN treatment group received a single intraperitoneal injection of 500 μL saline including PDRN (8 mg/kg) 1 h after ALI induction. To confirm the involvement of the adenosine A2A receptor in PDRN, 8 mg/kg 7-dimethyl-1-propargylxanthine (DMPX) was applied with PDRN treatment. Rats were then sacrificed 12 h after PDRN and DMPX treatments. Intratracheal administration of LPS caused lung tissue damage and significantly increased the lung injury scores and levels of pro-inflammatory cytokines, and apoptotic factors. In addition, MAPK/NF-κB signaling factors were increased by ALI initiation. PDRN treatment potently suppressed expressions of MAPK/NF-κB signaling factors compared to the PDRN + DMPX co-treated group. These alterations led to a reduction of pro-inflammatory cytokines, apoptotic factors, and NF-κB and MAPK signaling, which promoted the recovery of damaged lung tissue. PDRN therapy demonstrated therapeutic effects for LPS-induced ALI compared to the non-treated and DMPX-treated groups. Therefore, PDRN may be used as a therapy for initial treatment of ALI. Highlights Initiation of ALI is release of inflammatory mediators. During the onset of ALI promotes apoptosis, which increase tissue damage. Inflammation and apoptosis by ALI is related to MAPK/NF-κB signaling pathway. PDRN modulates MAPK/NF-κB signaling pathway to inhibit apoptosis and inflammation. PDRN may serve as a new therapeutic option in the initial treatment of ALI. Graphical abstract [DISPLAY OMISSION]

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Polydeoxyribonucleotide ameliorates lipopolysaccharide-induced acute lung injury via modulation of the MAPK/NF-κB signaling pathway in rats

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Polydeoxyribonucleotide ameliorates lipopolysaccharide-induced acute lung injury via modulation of the MAPK/NF-κB signaling pathway in rats

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