title: Infliximab attenuates activated charcoal and polyethylene glycol aspiration-induced lung injury in rats.
abstract: Aspiration is a serious complication of gastrointestinal (GI) decontamination procedure. Studies have shown that tumor necrosis factor-α (TNF-α) blockers have beneficial effects on lung injury. Therefore, the authors investigated the attenuation by infliximab (INF) on activated charcoal (AC)- and polyethylene glycol (PEG)-induced lung injury in rat model. Forty-two male Sprague-Dawley rats were allotted into 1 of 6 groups: saline (NS), activated charcoal (AC), polyethylene glycol (PEG), NS+INF treated, AC+INF treated, and PEG+INF treated. All materials were aspirated into the lungs at a volume of 1 mL/kg. Before aspiration, the rats were injected subcutaneously with INF. Seven days later, both lungs and serum specimens in all groups were evaluated histopathologically, immunohistochemically, and biochemically. Following aspiration of AC and PEG, evident histopathological changes were assigned in the lung tissue that were associated with increased expression of inducible nitric oxide synthase (iNOS), increased serum levels of oxidative stress markers (malondialdehyde [MDA], surfactant protein-D [SP-D], TNF-α), and decreased antioxidant enzyme (glutathione peroxidase [GSH-Px]) activities. INF treatment significantly decreased the elevated serum MDA and TNF-α levels and increased serum GSH-Px levels. Furthermore, the current results show that there is a significant reduction in the activity of iNOS in lung tissue and increased serum SP-D levels of AC and PEG aspiration-induced lung injury with INF treatment. These findings suggest that INF attenuates lung inflammation and prevents GI decontamination agent-induced lung injury in rats.
authors.affiliation: Department of Chest Disease, Samsun Chest Disease and Chest Surgery Hospital, Samsun, Turkey. aygulguzel1977@hotmail.com
authors.forename: Aygül
authors.initials: A
authors.lastname: Güzel
authors.forename: Mithat
authors.initials: M
authors.lastname: Günaydin
authors.forename: Ahmet
authors.initials: A
authors.lastname: Güzel
authors.forename: Hasan
authors.initials: H
authors.lastname: Alaçam
authors.forename: Naci
authors.initials: N
authors.lastname: Murat
authors.forename: Ayhan
authors.initials: A
authors.lastname: Gacar
authors.forename: Tolga
authors.initials: T
authors.lastname: Güvenç
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D002606:Charcoal / Q000633:toxicity*; D005765:Gastrointestinal Agents / Q000009:adverse effects; D005979:Glutathione Peroxidase / Q000378:metabolism; D000069285:Infliximab; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D055370:Lung Injury / Q000139:chemically induced* / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D011014:Pneumonia / Q000188:drug therapy / Q000378:metabolism; D011092:Polyethylene Glycols / Q000633:toxicity*; D037663:Pulmonary Surfactant-Associated Protein D / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D005765:Gastrointestinal Agents; D037663:Pulmonary Surfactant-Associated Protein D; D014409:Tumor Necrosis Factor-alpha; D002606:Charcoal; D011092:Polyethylene Glycols; D008315:Malondialdehyde; D000069285:Infliximab; D005979:Glutathione Peroxidase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat