NDLI: Vitamin $K_{3}$ attenuates lipopolysaccharide-induced acute lung injury through inhibition of nuclear factor-κB activation

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Vitamin $K_{3}$ attenuates lipopolysaccharide-induced acute lung injury through inhibition of nuclear factor-κB activation

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tanaka, S. Nishiumi, S. Nishida, M. Mizushina, Y. Kobayashi, K. Masuda, A. Fujita, T. Morita, Y. Mizuno, S. Kutsumi, H. Azuma, T. Yoshida, M.
Description	Country affiliation: Japan Author Affiliation: Tanaka S ( Division of Gastroenterology, Department of Internal Medicine, Graduate School of Medicine, Kobe University, Kusunoki-Cho, Hyogo, Japan.)
Abstract	Vitamin K is a family of fat-soluble compounds including phylloquinone (vitamin K1), menaquinone (vitamin K2) and menadione (vitamin K3). Recently, it was reported that vitamin K, especially vitamins K1 and K2, exerts a variety of biological effects, and these compounds are expected to be candidates for therapeutic agents against various diseases. In this study, we investigated the anti-inflammatory effects of vitamin K3 in in vitro cultured cell experiments and in vivo animal experiments. In human embryonic kidney (HEK)293 cells, vitamin K3 inhibited the tumour necrosis factor (TNF)-alpha-evoked translocation of nuclear factor (NF)-kappaB into the nucleus, although vitamins K1 and K2 did not. Vitamin K3 also suppressed the lipopolysaccharide (LPS)-induced nuclear translocation of NF-kappaB and production of TNF-alpha in mouse macrophage RAW264.7 cells. Moreover, the addition of vitamin K3 before and after LPS administration attenuated the severity of lung injury in an animal model of acute lung injury/acute respiratory distress syndrome (ARDS), which occurs in the setting of acute severe illness complicated by systemic inflammation. In the ARDS model, vitamin K3 also suppressed the LPS-induced increase in the serum TNF-alpha level and inhibited the LPS-evoked nuclear translocation of NF-kappaB in lung tissue. Despite marked efforts, little therapeutic progress has been made, and the mortality rate of ARDS remains high. Vitamin K3 may be an effective therapeutic strategy against acute lung injury including ARDS.
File Format	HTM / HTML
ISSN	00099104
e-ISSN	13652249
DOI	10.1111/j.1365-2249.2009.04083.x
Journal	Clinical & Experimental Immunology
Issue Number	2
Volume Number	160
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2010-05-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Immunology Acute Lung Injury Drug Therapy Anti-inflammatory Agents, Non-steroidal Therapeutic Use Lipopolysaccharides Toxicity Nf-kappa B Antagonists & Inhibitors Vitamin K 3 Chemically Induced Genetics Metabolism Animals Pharmacology Bronchoalveolar Lavage Fluid Cytology Cells, Cultured Drug Effects Drug Evaluation, Preclinical Gene Expression Regulation Kidney Lung Immunology Pathology Macrophages, Peritoneal Mice Mice, Inbred C57bl Neutrophils Tumor Necrosis Factor-alpha Biosynthesis Secretion Vitamin K 1 Vitamin K 2 Comparative Study Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Vitamin $K_{3}$ attenuates lipopolysaccharide-induced acute lung injury through inhibition of nuclear factor-κB activation