Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/30014
Title: The effects of bosentan on hyperoxia-induced lung injury in neonatal rats
Authors: Özdemir, Özmert M.A.
Taban, Özgün
Enli, Yaşar
Bir, Ferda
Şahin, Barbaros
Ergin, Hacer
Keywords: bosentan
hyperoxia-induced lung injury
treatment
interleukin 10
interleukin 1beta
interleukin 6
smooth muscle actin
tumor necrosis factor
actin
biological marker
endothelin receptor antagonist
smooth muscle actin, rat
animal experiment
animal tissue
Article
body weight
comparative study
controlled study
drug effect
histopathology
lung fibrosis
lung parenchyma
newborn
nonhuman
pneumonia
priority journal
protein blood level
rat
respiratory tract disease assessment
surface area
animal
biosynthesis
complication
disease model
hyperoxia
immunohistochemistry
intraperitoneal drug administration
lung
lung injury
metabolism
pathology
treatment outcome
Wistar rat
Actins
Animals
Animals, Newborn
Biomarkers
Bosentan
Disease Models, Animal
Endothelin Receptor Antagonists
Hyperoxia
Immunohistochemistry
Injections, Intraperitoneal
Lung
Lung Injury
Rats
Rats, Wistar
Treatment Outcome
Publisher: Blackwell Publishing
Abstract: Background: Bronchopulmonary dysplasia (BPD) remains an important cause of morbidity and mortality in premature infants. There is currently no proven effective treatment modality for BPD, and inflammation and oxidative injury play an important role in the pathogenesis of this disease. This study investigated the histopathological and biochemical effects of bosentan, which is a non-specific endothelin receptor antagonist with known antioxidant and anti-inflammatory properties, on hyperoxia-induced lung injury (HILI) in neonatal rats. Methods: The experiment was performed on newborn rats from the 3rd to the 13th postnatal day. The rats were randomly divided into six groups: Group 1 (air-exposed + saline, n = 6); Group 2 (HILI, n = 8); Group 3 (air-exposed + bosentan, n = 7); Group 4 (HILI + saline, n = 7); Group 5 (HILI + early bosentan-treated group, n = 6), and Group 6 (HILI + late bosentan-treated group, n = 7). Bosentan was administered (30 mg/kg/day) intraperitoneally. The histopathological effects of bosentan on lung tissue were assessed by their alveolar surface area, fibrosis, and smooth muscle actin (SMA) scores, and the biochemical effects on lung tissue were assessed by interleukin-1 beta (IL-1ß), IL-6, IL-10, and tumor necrosis factor-alpha (TNF-?). Results: The alveolar surface area and fibrosis scores were found to be significantly higher in HILI groups compared with Group 1 (P < 0.01). The SMA scores in HILI groups were also significantly higher than Group 1 (P < 0.01). Bosentan treatment, especially late therapy, reduced all of these histopathological scores and the levels of IL-6 and TNF-? in the hyperoxia groups (P < 0.01). Conclusion: This experimental study showed that bosentan had a protective effect on hyperoxic lung injury through its anti-inflammatory properties. © 2019 Japan Pediatric Society
URI: https://hdl.handle.net/11499/30014
https://doi.org/10.1111/ped.14013
ISSN: 1328-8067
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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