Arctiin Prevents LPS-Induced Acute Lung Injury via Inhibition of PI3K/AKT Signaling Pathway in Mice

支气管肺泡灌洗 蛋白激酶B PI3K/AKT/mTOR通路 髓过氧化物酶 脂多糖 药理学 化学 炎症 NF-κB 医学 信号转导 免疫学 内科学 生物化学
作者
Bo Zhou,Guohu Weng,Zhengxin Huang,Tao Liu,Feiyue Dai
出处
期刊:Inflammation [Springer Nature]
卷期号:41 (6): 2129-2135 被引量:35
标识
DOI:10.1007/s10753-018-0856-x
摘要

Arctiin is a lignin isolated from Arctium lappa which has been known to have anti-viral and anti-inflammatory effects. The aim of this study is to explore the protective effect of arctiin on lipopolysaccharide (LPS)-induced inflammatory responses in acute lung injury (ALI) model of mice. Male BALB/c mice were pretreated with commercial arctiin (10, 20, and 40 mg/kg) 1 h prior to LPS challenge. Twelve hours later, airway inflammation was assessed. We assessed the effects of arctiin on the LPS-induced production of TNF-α, IL-6, and IL-1β in the bronchoalveolar lavage fluid (BALF). The lung wet-to-dry weight ratio, myeloperoxidase (MPO) activity, and inflammatory signaling pathway were also detected. Our results showed that arctiin not only significantly ameliorated LPS-stimulated lung histopathological changes but also reduced the lung MPO activity. Arctiin also dramatically decreased the production of TNF-α, IL-1β, and IL-6 in the BALF. In addition, arctiin significantly inhibited LPS-induced PI3K/Akt phosphorylation as well as NF-κB activation. In conclusion, our results suggested that arctiin protected against LPS-induced ALI through inhibiting PI3K/AKT/NF-κB signaling pathway.
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