Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2014 Sep;5(9):2106-12.
doi: 10.1039/c4fo00384e.

Inhibition of allergic airway inflammation through the blockage of NF-κB activation by ellagic acid in an ovalbumin-induced mouse asthma model

Affiliations

Inhibition of allergic airway inflammation through the blockage of NF-κB activation by ellagic acid in an ovalbumin-induced mouse asthma model

Ershun Zhou et al. Food Funct. 2014 Sep.

Abstract

Allergic asthma is a complex inflammatory disease characterized by airway hyperresponsiveness, eosinophilic inflammation and the hypersecretion of mucus by goblet cells. Ellagic acid (EA), a natural polyphenolic compound present as ellagitannins in fruits and fruit juices, has been reported to show potent anti-inflammatory properties in various diseases. We aimed to investigate the effects of EA in an ovalbumin (OVA)-induced mouse asthma model and to explore its potential mechanism of action. Our results showed that EA resulted in a significant reduction in lung eosinophilia, increased Th2 cytokines in bronchoalveolar lavage fluid and increased OVA-induced specific IgE in serum samples. Moreover, histological examination showed that EA markedly inhibited lung eosinophilic inflammation and goblet cell hyperplasia. In addition, EA attenuated the development of airway hyperresponsiveness and blocked NF-κB activation. These results demonstrate that EA shows obvious anti-inflammatory effects in OVA-induced asthma in a mouse model, possibly through inhibiting NF-κB activation. Therefore it may be a potential therapeutic agent for the treatment of allergic asthma.

PubMed Disclaimer

Similar articles

Cited by