Effect Of1,25（OH）₂D₃on Hyperoxia-induced Lung Injury In Neonatal Rats

ObjectiveTo investigate the effect of1,25(OH)2D3on expression of TLR4/NF-κB signaling in hyperoxia-induced lung injury of neonatal rats and to investigate the effect of1,25(OH)2D3on hyperoxia-induced lung injury in neonatal rats.MethodNewborn Sprague-Dawley rats were pooled together within12hours after birth and randomly divided into three groups:I air group II hyperoxia group and III hyperoxia+1,25(OH)2D3group. Group I rats were exposed to air, Group II and III rats were exposed to hyperoxia (>85%oxygen).Group III rats were injected1,25(OH)2D3(0.5μg/(kg·d)) intraperitoneally once a day and they had been given for7days; meanwhile group I and II rats received0.9%saline in the same way.All rats were killed on day7. Lung tissue sections were stained by haematoxylin and eosin in order to assess lung histologic changes and examine lung RAC. The expression of TLR4and phosphorylated NF-κB p65in the lung were determined with Western blot.The levels of TLR4、TNF-α、IL-1β、IL-6mRNA were measured by Real time-PCR.Results1. After7days, the weight of rats in hyperoxia group showed significant decrease compared with that in air group (P<0.05); however, the weight of rats in1,25(OH)2D3group significantly increased compared with that in hyperoxia group (P <0.05). 2. After7days, compared with air group rats, rats in hyperoxia group showed signifi-cant lung injury, which was characterized by alveolitis and delayed development of lung, as well as decreased RAC. However,1,25(OH)2D3significantly attenuated hyperoxia-induced lung injury.3. Compared with air group, the expression of TLR4and phosphorylated NF-κB p65protein in the lung tissue significantly increased in hyperoxia group (P<0.05), but the expression was lower in1,25(OH)2D3group compared with hyperoxia group (P<0.05).4. Compared with air group, the expression of TLR4n TNF-α、IL-1β and IL-6mRNA in lung tissue significantly increased in hyperoxia group (P<0.05), but the expression was lower in1,25(OH)2D3group compared with hyperoxia group (P<0.05).Conclusion1,25(OH)2D3treatment can attenuate hyperoxia-induced lung injury, which may be related to downregulating of TLR4/NF-κB signaling.