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Evidence-Based Complementary and Alternative Medicine
Volume 2012, Article ID 383608, 8 pages
http://dx.doi.org/10.1155/2012/383608
Research Article

Luteolin Suppresses Inflammatory Mediator Expression by Blocking the Akt/NFκB Pathway in Acute Lung Injury Induced by Lipopolysaccharide in Mice

1Department of Pharmacology, School of Medicine, Chung Shan Medical University, No. 110, Sec.1, Jianguo N. Road, Taichung 40201, Taiwan
2Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan
3Department of Neurology, Show Chwan Memorial Hospital, Changhua, Taiwan
4Graduate Institute of Life Sciences, National Chung Hsing University, Taichung, Taiwan
5Department of Anatomy, School of Medicine, Chung Shan Medical University, No. 110, Sec.1, Jianguo N. Road, Taichung 40201, Taiwan

Received 20 July 2011; Revised 9 September 2011; Accepted 9 September 2011

Academic Editor: Bashar Saad

Copyright © 2012 Yi-Ching Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Acute lung injury (ALI), instilled by lipopolysaccharide (LPS), is a severe illness with excessive mortality and has no specific treatment strategy. Luteolin is an anti-inflammatory flavonoid and widely distributed in the plants. Pretreatment with luteolin inhibited LPS-induced histological changes of ALI and lung tissue edema. In addition, LPS-induced inflammatory responses, including increased vascular permeability, tumor necrosis factor (TNF)-α and interleukin (IL)-6 production, and expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), were also reduced by luteolin in a concentration-dependent manner. Furthermore, luteolin suppressed activation of NFκB and its upstream molecular factor, Akt. These results suggest that the protection mechanism of luteolin is by inhibition of NFκB activation possibly via Akt.