Atractylenolide I protects mice from lipopolysaccharide-induced acute lung injury

被引:45
作者
Zhang, Jun-liang [1 ]
Huang, Wei-min [1 ]
Zeng, Qi-yi [2 ]
机构
[1] Southern Med Univ, Dept Neonatol, Nanfang Hosp, Guangzhou 510515, Guangdong, Peoples R China
[2] Southern Med Univ, Ctr Pediat, Zhujiang Hosp, Guangzhou 510280, Guangdong, Peoples R China
关键词
Atractylenolide I; LPS; Acute lung injury; TLR4; NF-kappa B; NF-KAPPA-B; INFLAMMATORY RESPONSES; PATHWAY; MAPK; PATHOPHYSIOLOGY; MACROPHAGES; NEUTROPHILS; PREVENTION; LETHALITY; CYTOKINE;
D O I
10.1016/j.ejphar.2015.08.022
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Atractylenolide I (AO-I), one of the major bioactive components isolated from Rhizoma Atractylodes macrocephala, has been reported to have anti-inflammatory effects. In the present study, we investigated the protective effects of AO-I on acute lung injury (ALI) using LPS-induced ALI mouse model. Lung injury was assessed by histological study. Inflammatory cytokines TNF-alpha, IL-6 and IL-1 beta production were detected by ELISA. TLR4 expression and NF-kappa B activation were measured by western blot analysis. The results showed that treatment of AO-I significantly attenuated LPS-induced lung wet-to-dry weight ratio and MPO activity. Meanwhile, treatment of AO-I significantly inhibited the production of TNF-alpha, IL-6, IL-1 1 beta, IL-13, and MIF production in bronchoalveolar lavage fluid (BALF), as well as neutrophils and macrophages in BALE. AO-1 could up-regulate the production of IL-10 in BALF. Besides, LPS-induced TLR4 expression and NF-kappa B activation were suppressed by treatment of AO-I. In conclusion, the current study suggested that AO-I protected mice acute lung injury induced by LPS via inhibition of TLR4 expression and NF-kappa B activation. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:94 / 99
页数:6
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