Budesonide ameliorates lung injury induced by large volume ventilation.
Budesonide ameliorates lung injury induced by large volume ventilation.
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DOI：
10.1186/s12890-016-0251-z
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发表时间：
2016-06-04
影响因子：
3.1
通讯作者：
Wang GN
中科院分区：
文献类型：
--
作者：
Ju YN;Yu KJ;Wang GN
呼吸机诱导的肺损伤（VILI）是急性呼吸功能障碍综合征患者的健康问题。本研究的目的是探讨布地奈德治疗VILI的有效性。将24只大鼠随机分为3组：机械通气组、机械通气/布地奈德组和假手术组，机械通气后立即以30 ml/kg潮气量通气或仅麻醉4 h或生理盐水或布地奈德气道滴注。检测支气管肺泡灌洗液（BALF）中PaO 2/FiO 2、湿干重比、蛋白浓度、中性粒细胞计数、中性粒细胞弹性蛋白酶水平及炎症相关因子水平。肺组织学观察及细胞凋亡测定.与机械通气组相比，布地奈德治疗后PaO 2/FiO 2比值明显升高。布地奈德组肺湿干重比、总蛋白、中性粒细胞弹性蛋白酶水平和BALF中嗜中性粒细胞计数均降低。布地奈德组BALF和血浆肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1β、IL-6、细胞间粘附分子（ICAM）-1和巨噬细胞炎性蛋白（MIP）-2水平降低，而IL-10水平升高。布地奈德可抑制肺组织磷酸化核因子（NF）-κ B水平。布地奈德治疗可减轻肺组织学改变和细胞凋亡。Bax、caspase-3和切割的caspase-3被下调，Bcl-2被上调。布地奈德改善大容量通气引起的肺损伤，可能是通过改善上皮通透性，减轻水肿，抑制局部和全身炎症，减少VILI细胞凋亡。
Ventilation-induced lung injury (VILI) is a health problem for patients with acute respiratory dysfunction syndrome. The aim of this study was to investigate the effectiveness of budesonide in treating VILI. Twenty-four rats were randomized to three groups: a ventilation group, ventilation/budesonide group, and sham group were ventilated with 30 ml/kg tidal volume or only anesthesia for 4 hor saline or budesonide airway instillation immediately after ventilation. The PaO2/FiO2and wet-to-dry weight ratios, protein concentration, neutrophil count, and neutrophil elastase levels in bronchoalveolar lavage fluid (BALF) and the levels of inflammation-related factors were examined. Histological evaluation of and apoptosis measurement inthe lung were conducted. Compared with that in the ventilation group, the PaO2/FiO2 ratio was significantly increased by treatment with budesonide. The lung wet-to-dry weight ratio, total protein, neutrophil elastase level, and neutrophilcount in BALF were decreased in the budesonide group. The BALF and plasma tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, intercellular adhesion molecule (ICAM)-1, and macrophage inflammatory protein (MIP)-2 levels were decreased, whereas the IL-10 level was increased in the budesonide group. The phosphorylated nuclear factor (NF)-kBlevels in lung tissue were inhibited by budesonide. The histological changes in the lung and apoptosis were reduced by budesonide treatment. Bax, caspase-3, and cleaved caspase-3 were down-regulated, and Bcl-2 was up-regulated by budesonide. Budesonide ameliorated lung injury induced by large volume ventilation, likely by improving epithelial permeability, decreasing edema, inhibiting local and systemic inflammation, and reducing apoptosis in VILI.