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
相关论文
共 31 条
[1]  
[Anonymous], 2014, J FUNDAM RENEW ENERG
[2]   Targeted disruption of migration inhibitory factor gene reveals its critical role in sepsis [J].
Bozza, M ;
Satoskar, AR ;
Lin, GS ;
Lu, B ;
Humbles, AA ;
Gerard, C ;
David, JR .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (02) :341-346
[3]   High incidence of acute lung injury in children with Down syndrome [J].
Bruijn, M. ;
van der Aa, L. B. ;
van Rijn, R. R. ;
Bos, A. P. ;
van Woensel, J. B. M. .
INTENSIVE CARE MEDICINE, 2007, 33 (12) :2179-2182
[4]   Epidemiology and outcome of acute lung injury in European intensive care units - Results from the ALIVE study [J].
Brun-Buisson, C ;
Minelli, C ;
Bertolini, G ;
Brazzi, L ;
Pimentel, J ;
Lewandowski, K ;
Bion, J ;
Rornand, JA ;
Villar, J ;
Thorsteinsson, A ;
Damas, P ;
Armaganidis, A ;
Lemaire, FO .
INTENSIVE CARE MEDICINE, 2004, 30 (01) :51-61
[5]   Gamma-irradiated resveratrol negatively regulates LPS-induced MAPK and NF-κB signaling through TLR4 in macrophages [J].
Byun, Eui-Baek ;
Sung, Nak-Yun ;
Park, Jae-Nam ;
Yang, Mi-So ;
Park, Sang-Hyun ;
Byun, Eui-Hong .
INTERNATIONAL IMMUNOPHARMACOLOGY, 2015, 25 (02) :249-259
[6]   The role of inflammation in the pathophysiology of CF lung disease [J].
Chmiel, JF ;
Berger, M ;
Konstan, MW .
CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY, 2002, 23 (01) :5-27
[7]   LPS-TLR4 signaling to IRF-3/7 and NF-κB involves the toll adapters TRAM and TRIF [J].
Fitzgerald, KA ;
Rowe, DC ;
Barnes, BJ ;
Caffrey, DR ;
Visintin, A ;
Latz, E ;
Monks, B ;
Pitha, PM ;
Golenbock, DT .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 198 (07) :1043-1055
[8]   Lung pathology of severe acute respiratory syndrome (SARS): A study of 8 autopsy cases from Singapore [J].
Franks, TJ ;
Chong, PY ;
Chui, P ;
Galvin, JR ;
Lourens, RM ;
Reid, AH ;
Selbs, E ;
McEvoy, PL ;
Hayden, DL ;
Fukuoka, J ;
Taubenberger, JK ;
Travis, WD .
HUMAN PATHOLOGY, 2003, 34 (08) :743-748
[9]   INTERLEUKIN-10 REDUCES THE RELEASE OF TUMOR-NECROSIS-FACTOR AND PREVENTS LETHALITY IN EXPERIMENTAL ENDOTOXEMIA [J].
GERARD, C ;
BRUYNS, C ;
MARCHANT, A ;
ABRAMOWICZ, D ;
VANDENABEELE, P ;
DELVAUX, A ;
FIERS, W ;
GOLDMAN, M ;
VELU, T .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 177 (02) :547-550
[10]   NF-κB and rel proteins:: Evolutionarily conserved mediators of immune responses [J].
Ghosh, S ;
May, MJ ;
Kopp, EB .
ANNUAL REVIEW OF IMMUNOLOGY, 1998, 16 :225-260