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The effects of bosentan on hyperoxia-induced lung injury in neonatal rats
Özmert Ma Özdemir1, Özgün Taban2, Yaşar Enli3
1Division of Neonataology, Pamukkale University, Denizli, Turkey.
Insights
Bosentan demonstrates protective effects against hyperoxia-induced lung injury in neonatal rats by reducing inflammation and improving lung tissue. This finding offers potential therapeutic avenues for bronchopulmonary dysplasia.
Area of Science:
- Neonatal Medicine
- Pulmonary Research
- Pharmacology
Background:
- Bronchopulmonary dysplasia (BPD) is a significant cause of premature infant mortality.
- Current treatments for BPD lack proven efficacy.
- Inflammation and oxidative stress are key contributors to BPD pathogenesis.
Purpose of the Study:
- To investigate the effects of bosentan on hyperoxia-induced lung injury (HILI) in neonatal rats.
- To assess the histopathological and biochemical impacts of bosentan.
- To evaluate bosentan's antioxidant and anti-inflammatory properties in this model.
Main Methods:
- Neonatal rats were exposed to hyperoxia from postnatal day 3 to 13.
- Rats received saline or bosentan (30 mg/kg/day) via intraperitoneal injection.
- Lung tissue was analyzed for alveolar surface area, fibrosis, smooth muscle actin (SMA), and inflammatory cytokines (IL-1β, IL-6, IL-10, TNF-α).
Main Results:
- Hyperoxia-induced lung injury significantly increased alveolar surface area, fibrosis, and SMA scores.
- Bosentan treatment, particularly late-stage therapy, significantly reduced these histopathological markers.
- Bosentan also decreased elevated levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in hyperoxia-exposed rats.
Conclusions:
- Bosentan exhibits a protective effect against hyperoxia-induced lung injury in a neonatal rat model.
- The anti-inflammatory properties of bosentan contribute to its therapeutic potential.
- These findings suggest bosentan as a potential treatment for conditions like bronchopulmonary dysplasia.
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-1β), IL-6, IL-10, and tumor necrosis factor-alpha (TNF-α).
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-α 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.
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