Abstract

Preterm infants have risks of developing vitamin D deficiency. Thus we aimed to investigate the effect of vitamin D on hyperoxia-induced lung injury in newborn rats. Full term rat pups were included in the study 12-24 hr after delivery. The pups were randomly divided into eight groups as follows: normoxia control group (NC), normoxia plus vitamin D group (ND1, 1 ng/gr/day vitamin D), normoxia plus vitamin D group (ND2, 3 ng/gr/day vitamin D), normoxia plus vitamin D group (ND3, 5 ng/gr/day vitamin D), hyperoxia control group (HC), hyperoxia plus vitamin D group (HD1, 1 ng/gr/day vitamin D), hyperoxia plus Vitamin D group (HD2, 3 ng/gr/day vitamin D), hyperoxia plus vitamin D group (HD3, 5 ng/gr/day vitamin D). The histopathological effects of vitamin D were assessed by alveolar surface area (with mean linear intercept (MLI) method), apoptosis index and proliferating cell nuclear antigen (PCNA) index. MLI values were significantly lower among three groups (HD1: 83.93 ± 1.95 μm, HD2: 81.76 ± 1.68 μm, and HD3: 82.33 ± 1.87 μm) when compared with HC group (92.98 ± 2.09 μm) (P = 0.001, P = 0.0004, P = 0.002, respectively). Apoptotic cell index were significantly lower among three treatment groups (HD1: 1.455 ± 0.153, HD2: 0.575 ± 0.079, and HD3: 0.700 ± 0.105) when compared with HC group (2.500 ± 0.263) (P = 0.001, P = 0.001, P = 0.001, respectively). Although PCNA positive cell index did not change in HD1 group (0.132 ± 0.008) (P > 0.05), there were significant increases in HD2 (0.277 ± 0.026) and HD3 (0.266 ± 0.018) group when compared with HC group (0.142 ± 0.010) (HD2 P = 0.001, HD3 P = 0.001). Vitamin D seems to protect hyperoxia-induced lung injury in newborn rats. Pediatr Pulmonol. 2017;52:69-76. © 2016 Wiley Periodicals, Inc.

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