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Clausena anisata-mediated protection against lipopolysaccharide-induced acute lung injury in mice

Authors :
Do-Van Hai
Jung Hee Kim
Pyung-Keun Myung
Tran-The Bach
Na-Rae Shin
In-Sik Shin
Kyung-Seop Ahn
Sangho Choi
Ju-Mi Hong
Joongku Lee
Ok-Kyoung Kwon
Sei-Ryang Oh
Bui-Hong Quang
Chan-Mi Jeon
Source :
International journal of molecular medicine. 37(4)
Publication Year :
2015

Abstract

Clausena anisata (Willd.) Hook.f. ex Benth. (CA), which is widely used in traditional medicine, reportedly exerts antitumor, anti-inflammatory and other important therapeutic effects. The aim of the present study was to investigate the potential therapeutic effects of CA in a mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) and in LPS-stimulated RAW 264.7 cells. Male C57BL/6 mice were administered treatments for 3 days by oral gavage. On day 3, the mice were instilled intranasally with LPS or PBS followed 3 h later by oral CA (30 mg/kg) or vehicle administration. In vitro, CA decreased nitric oxide (NO) production and pro-inflammatory cytokines, such as interleukin (IL)-6 and prostaglandin E2 (PGE2), in LPS-stimulated RAW 264.7 cells. CA also reduced the expression of pro-inflammatory mediators, such as cyclooxygenase-2. In vivo, CA administration significantly reduced inflammatory cell numbers in the bronchoalveolar lavage fluid (BALF) and suppressed pro-inflammatory cytokine levels, including tumor necrosis factor-α (TNF-α), IL-6, and IL-1β, as well as reactive oxygen species production in the BALF. CA also effectively reduced airway inflammation in mouse lung tissue of an LPS-induced ALI mouse model, in addition to decreasing inhibitor κB (IκB) and nuclear factor-κB (NF-κB) p65 phosphorylation. Taken together, the findings demonstrated that CA inhibited inflammatory responses in a mouse model of LPS-induced ALI and in LPS-stimulated RAW 264.7 cells. Thus, CA is a potential candidate for development as an adjunctive treatment for inflammatory disorders, such as ALI.

Details

ISSN :
1791244X
Volume :
37
Issue :
4
Database :
OpenAIRE
Journal :
International journal of molecular medicine
Accession number :
edsair.doi.dedup.....3f3144977efcc3bd8b0ea63f52534693