Kuzubova N A, Lebedeva E S, Dvorakovskaya I V, Preobrazhenskaya T N, Surkova E A, Titova O N
Ross Fiziol Zh Im I M Sechenova. 2016 Jul;102(7):825-32.
Effect of mast cell degranulation blockade on the inflammatory response and character of the lung tissue structure-functional changes were evaluated in the chronic obstructive pulmonary disease model produced in rats by 60-day intermittent exposure to nitrogen dioxide. The membrane stabilizer sodium cromoglicate was used to blockade of mast cell degranulation. Lung tissue sections were stained with toluidine blue to identify mast cells. Bronchoalveolar lavage fluid (BALF) cytogram was determined. The levels of mast cell tryptase and chymase, proinflammatory cytokine TNF-α, surfactant protein B were measured in BALF. Suppression of mast cell degranulation prevented the release of proteases in the bronchoalveolar space and reduced activity of the inflammatory process. The influx of inflammatory cells and TNF-α concentration decreased. There was no interstitial inflammatory infiltration. Bronchoalveolar epithelium structure was recovered that is the basis of its functional usefulness. The results confirm the active involvement of mast cells in the development of the inflammatory process in obstructive pulmonary diseases and allow us to consider them as a possible therapeutic target.
在通过60天间歇性暴露于二氧化氮建立的大鼠慢性阻塞性肺疾病模型中,评估了肥大细胞脱颗粒阻断对炎症反应以及肺组织结构-功能变化特征的影响。使用膜稳定剂色甘酸钠来阻断肥大细胞脱颗粒。用甲苯胺蓝对肺组织切片进行染色以识别肥大细胞。测定支气管肺泡灌洗液(BALF)细胞图谱。测量BALF中肥大细胞类胰蛋白酶和糜酶、促炎细胞因子TNF-α、表面活性蛋白B的水平。肥大细胞脱颗粒的抑制阻止了支气管肺泡腔内蛋白酶的释放,并降低了炎症过程的活性。炎症细胞的流入和TNF-α浓度降低。没有间质炎症浸润。支气管肺泡上皮结构得以恢复,这是其功能有效性的基础。结果证实肥大细胞积极参与阻塞性肺疾病炎症过程的发展,并使我们能够将它们视为可能的治疗靶点。