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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 767689, 14 pages
http://dx.doi.org/10.1155/2013/767689
Research Article

Galangin Abrogates Ovalbumin-Induced Airway Inflammation via Negative Regulation of NF- B

1Department of Respiratory Medicine, The First Affiliated Hospital, Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, China
2Department of Respiratory Medicine, The Second Affiliated Hospital, Nanjing Medical University, 121 Jiangjiayuan Road, Nanjing 210011, China
3Department of Pathology, The First Affiliated Hospital, Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, China

Received 31 January 2013; Revised 14 April 2013; Accepted 25 April 2013

Academic Editor: Shuang-En Chuang

Copyright © 2013 Wang-Jian Zha 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

Persistent activation of nuclear factor B (NF- B) has been associated with the development of asthma. Galangin, the active pharmacological ingredient from Alpinia galanga, is reported to have a variety of anti-inflammatory properties in vitro via negative regulation of NF- B. This study aimed to investigate whether galangin can abrogate ovalbumin- (OVA-) induced airway inflammation by negative regulation of NF- B. BALB/c mice sensitized and challenged with OVA developed airway hyperresponsiveness (AHR) and inflammation. Galangin dose dependently inhibited OVA-induced increases in total cell counts, eosinophil counts, and interleukin-(IL-) 4, IL-5, and IL-13 levels in bronchoalveolar lavage fluid, and reduced serum level of OVA-specific IgE. Galangin also attenuated AHR, reduced eosinophil infiltration and goblet cell hyperplasia, and reduced expression of inducible nitric oxide synthase and vascular cell adhesion protein-1 (VCAM-1) levels in lung tissue. Additionally, galangin blocked inhibitor of B degradation, phosphorylation of the p65 subunit of NF- B, and p65 nuclear translocation from lung tissues of OVA-sensitized mice. Similarly, in normal human airway smooth muscle cells, galangin blocked tumor necrosis factor- induced p65 nuclear translocation and expression of monocyte chemoattractant protein-1, eotaxin, CXCL10, and VCAM-1. These results suggest that galangin can attenuate ovalbumin-induced airway inflammation by inhibiting the NF- B pathway.