title: Dexpanthenol therapy reduces lung damage in a hyperoxic lung injury in neonatal rats.
abstract: OBJECTIVE
  Dexpanthenol (Dxp) plays a major role in cellular defense and in repair systems against oxidative stress and inflammatory response and it has not yet been evaluated in treatment of bronchopulmonary dysplasia (BPD). We tested the hypothesis that proposes whether Dxp decreases the severity of lung injury in an animal model of BPD.
  
  
  METHODS
  Forty rat pups were divided into four groups: control, control + Dxp, hyperoxia and hyperoxia + Dxp. All animals were processed for lung histology and tissue analysis. The degree of lung inflammation, oxidative and antioxidant capacity was assessed from lung homogenates.
  
  
  RESULTS
  Lung injury score and alveol diameter increased in the hyperoxia group (p < 0.001). Median level of malondialdehyde, total oxidant status and oxidative stress indexes was significantly higher in the hyperoxia group compared to the other groups. The median superoxide dismutase activity in the hyperoxia group was notably less than those of control + Dxp and hyperoxia + Dxp groups (p < 0.01). Similarly, lung catalase, glutathione (GSH) peroxidase and reduced GSH activities in the hyperoxia group were significantly lower than other groups. Furthermore, the hyperoxia + Dxp group had lower tumor necrosis factor-α and interleukin-1β median levels compared to the hyperoxia group (p = 0.007).
  
  
  CONCLUSIONS
  Dxp treatment results in less emphysematous change as well as decrease in inflammation and oxidative stress markers in an animal model of BPD.
authors.affiliation: a Division of Neonatology, Department of Pediatrics , Inonu University School of Medicine , Malatya , Turkey .
authors.forename: Ramazan
authors.initials: R
authors.lastname: Ozdemir
authors.affiliation: b Department of Pediatrics .
authors.forename: Gulsum
authors.initials: G
authors.lastname: Demirtas
authors.affiliation: c Department of Pharmacology .
authors.forename: Hakan
authors.initials: H
authors.lastname: Parlakpinar
authors.affiliation: d Department of Physiology , and.
authors.forename: Alaadin
authors.initials: A
authors.lastname: Polat
authors.affiliation: d Department of Physiology , and.
authors.forename: Kevser
authors.initials: K
authors.lastname: Tanbag
authors.affiliation: e Department of Histology and Embryology , Inonu University School of Medicine , Malatya , Turkey.
authors.forename: Elif
authors.initials: E
authors.lastname: Taslidere
authors.affiliation: a Division of Neonatology, Department of Pediatrics , Inonu University School of Medicine , Malatya , Turkey .
authors.forename: Ahmet
authors.initials: A
authors.lastname: Karadag
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D004353:Drug Evaluation, Preclinical; D005260:Female; D018496:Hyperoxia / Q000150:complications; D008168:Lung / Q000473:pathology; D055370:Lung Injury / Q000201:enzymology / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D018384:Oxidative Stress; D010205:Pantothenic Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use; D011247:Pregnancy; D011897:Random Allocation; D017208:Rats, Wistar
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D010205:Pantothenic Acid; C007288:dexpanthenol
keywords: Bronchopulmonary dysplasia; chronic lung disease; dexpanthenol; hyperoxia; hyperoxic lung injury; pantothenic acid