Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

被引:44
作者
Yao, Li [1 ]
Shi, Yongyan [1 ]
Zhao, Xinyi [1 ]
Hou, Ana [1 ]
Xing, Yujiao [1 ]
Fu, Jianhua [1 ]
Xue, Xindong [1 ]
机构
[1] China Med Univ, Shengjing Hosp, Dept Pediat, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
vitamin D; hyperoxia-induced lung injury; Toll-like receptor 4; apoptosis; bronchopulmonary dysplasia; NEWBORN RATS; BRONCHOPULMONARY DYSPLASIA; INDUCED COLITIS; ACTIVATION; INFLAMMATION; APOPTOSIS; PATHWAY; CELLS; MODULATION; D-3;
D O I
10.3892/ijmm.2017.2961
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
With considerable morbidity and mortality, bronchopulmonary dysplasia (BPD) is a focus of attention in neonatology. Hyperoxia-induced lung injury has long been used as a model of BPD. Among all the signaling pathways involved, Toll-like receptor 4 (TLR4) has been demonstrated to play an important role, and is known to be regulated by vitamin D. This study aimed at elucidating the effect of vitamin D on hyperoxia-induced lung injury and the role of TLR4 in the process. Vitamin D was administered to hyperoxia-treated neonatal rats to investigate changes in the morphology of lungs and expression of pro-inflammatory cytokines, apoptotic proteins and TLR4. Vitamin D attenuated hyperoxia-induced lung injury by protecting the integrity of the lung structure, decreasing extracellular matrix deposition and inhibiting inflammation. The upregulation of TLR4 by hyperoxia was ameliorated by vitamin D and apoptosis was reduced. Vitamin D administration antagonized the activation of TLR4 and therefore alleviated inflammation, reduced apoptosis and preserved lung structure.
引用
收藏
页码:1403 / 1408
页数:6
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