期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 642, 期 1-3, 页码 146-153出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2010.05.012
关键词
Icariin; RAW 264.7 macrophages cells; Phosphatidylinositol 3-kinase/amino kinase terminal (PI3K/Akt); NF-kappa B p65
资金
- National Basic Science Program of China [2009CB523000]
- Shanghai Science and Technology Committee [2009XD1400700]
- China Ministry of Education [200802461053]
This study aimed to investigate the mechanism underlying the attenuation of LPS-induced lung inflammation by icariin in vivo and in vitro. The anti-inflammatory effects of icariin on LPS-induced acute inflammatory and the molecular mechanism were investigated. Pretreatment with icarrin (20 mg/kg) could attenuate acute lung inflammation by inhibiting mRNA expressions of tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), metalloproteinase cycloxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in the lung of LPS-treated mice. In addition, icariin suppressed the secretion of TNF-alpha, prostaglandin E2 (PGE(2)) and nitric oxide (NO) as well as NF-kappa B p65 activation. Furthermore, decreased myeloperoxidase (MPO) activity was observed in the lung tissue and LPS-induced cytotoxicity in the RAW 264.7 macrophages cells was also markedly attenuated by icariin. Western blotting analysis and confocal microscopy showed that icariin pretreatment reduced the nucleus transportation and constant level of NF-kappa B p65 in the RAW 264.7 macrophage cells. However, the protective effects of icariin were reversed by a PI3K/Akt inhibitor (wortmannin). Our in vitro and in vivo results suggested that activation of the PI3K/Akt pathway and the inhibition of NF-kappa B were involved in the protective effects of icariin on LPS-induced acute inflammatory responses. (C) 2010 Elsevier B.V. All rights reserved.
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