Abstract
Abstract Persistent activation of nuclear factor (NF)-κB has been associated with the development of asthma. Andrographolide, the principal active component of a medicinal plant Andrographis paniculata, has been shown to inhibit NF-κB activity. We hypothesized that andrographolide may attenuate allergic asthma via inhibition of the NF-κB signaling pathway. BALB/c mice sensitized and challenged with OVA developed airway inflammation. Andrographolide inhibited OVA-induced increases in total cell count, eosinophil count, and IL-4, IL-5 and IL-13 levels in bronchoalveolar lavage fluid, and reduced serum level of OVA-specific IgE. It attenuated OVA-induced lung tissue eosinophilia and airway mucus production, mRNA expression of E-selectin, chitinases, Muc5ac and inducible nitric oxide synthase in lung tissues, and airway hyperresponsiveness to methacholine. In human lung epithelial cells, andrographolide blocked TNF-α-induced phosphorylation of inhibitory κB (IκB) kinase-β (IKKβ), and downstream IκBα degradation, p65 subunit of NF-κB phosphorylation, and p65 nuclear translocation and DNA-binding activity. Our findings implicate a potential therapeutic value of andrographolide in the treatment of asthma and it may act by inhibiting NF-κB pathway at the level of IKKβ activation. (This work was supported by a BioMedical Research Council grant BMRC06/1/21/19/443)
Published Version
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