Bronchopulmonary dysplasia (BPD) remains to be an important cause of morbidity and mortality in premature infants. Currently, there is no proven effective treatment modality for BPD, and inflammation and oxidative injury play an important role in the pathogenesis of this disease. Herein, the histopathological and biochemical effects of bosentan, which is a non-specific endothelin receptor antagonist and known antioxidant and anti-inflammatory properties, on hyperoxia-induced lung injury (HILI) model in neonatal rats were investigated.The experiment was performed on newborn rats from the 3 to 13 postnatal day and they 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 alveolar surface area, fibrosis, and smooth muscle actin (SMA) score, 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).The alveolar surface area and fibrosis scores were found to be significantly higher in HILI groups compared with Group 1 (p<0.01). SMA score in HILI group was 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).This experimental study showed that bosentan had a protective effect on hyperoxic lung injury through its anti-inflammatory properties.