卵清蛋白
PI3K/AKT/mTOR通路
支气管肺泡灌洗
免疫印迹
蛋白激酶B
H&E染色
肺
医学
免疫组织化学
信号转导
病理
免疫学
细胞生物学
生物
化学
内科学
免疫系统
基因
生物化学
作者
Xin Li,Ling Zhou,Zewen Zhang,Yuanyuan Liu,Ju Liu,Caiqing Zhang
标识
DOI:10.1080/01902148.2020.1740356
摘要
Purpose: Airway remodeling is one of the features of severe asthma. Previous study shows that IL-27 inhibits airway inflammation in asthmatic mice. However, the role of IL-27 on airway remodeling in OVA-induced asthmatic mice and its possible mechanism remain unclear. Methods: We established an ovalbumin (OVA)-induced asthmatic mice model. IL-27 were preventative administered to OVA-induced asthmatic mice. The total cells in Bronchoalveolar lavage fluid (BALF) and Airway hyperresponsiveness (AHR) were measured. The lung tissues were performed by Hematoxylin and eosin (HE) staining to estimate the pathological changes. Masson staining was used to observe the collagen deposition area. The expression of α-smooth muscle actin (α-SMA) and Type I collagen was measured by immunohistochemistry, western blot, and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Additionally, western blot was also used to measure the expression of phosphorylated-Akt (p-Akt) in each group. Results: IL-27 group showed significant inhibitory effect on the α-SMA and Type I collagen. The expression of p-Akt in the tissues of asthma model was increased and inhibited by IL-27. Conclusions: IL-27 can alleviate airway remodeling in OVA-induced asthmatic mice, and the mechanism may relate to PI3K/Akt pathway.
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