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

2011; Hindawi Publishing Corporation; Volume: 2012; Linguagem: Inglês

10.1155/2012/383608

1741-4288

Yi-Ching Li, Chung‐Hsin Yeh, Ming‐Ling Yang, Yu‐Hsiang Kuan,

Inflammasome and immune disorders

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 NF κ B and its upstream molecular factor, Akt. These results suggest that the protection mechanism of luteolin is by inhibition of NF κ B activation possibly via Akt.