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

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4.
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维生素 D 通过下调 Toll 样受体 4 减轻高氧引起的肺损伤

DOI:
10.3892/ijmm.2017.2961
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发表时间:
2017-06
影响因子:
5.4
通讯作者:
Xue X
Xue X
中科院分区:
医学3区
文献类型:
--
作者:
Yao L;Shi Y;Zhao X;Hou A;Xing Y;Fu J;Xue X

文献摘要

相似文献

支气管肺发育不良(BPD)的发病率和死亡率相当高,一直是泌尿外科关注的焦点。长期以来,高氧诱导的肺损伤一直被用作BPD的模型。在所有参与的信号通路中,Toll样受体4(TLR4)已被证明发挥重要作用,并且已知受维生素D调节。本研究旨在阐明维生素D对高氧肺损伤的影响及TLR4在此过程中的作用。给予维生素D高氧处理的新生大鼠,以研究肺的形态学和促炎细胞因子,凋亡蛋白和TLR4的表达的变化。维生素D通过保护肺结构的完整性、减少细胞外基质沉积和抑制炎症来减轻高氧诱导的肺损伤。维生素D可减轻高氧对TLR4的上调,并减少细胞凋亡。维生素D给药拮抗TLR4的活化,因此减轻炎症,减少细胞凋亡和保护肺结构。
With considerable morbidity and mortality, bron-chopulmonary 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.