Article Sidebar
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Trifolirhizin mitigates ovalbumin-induced lung inflammation and tissue damage in neonatal rats via inhibition of the NF-κB signaling pathway
Abstract
Purpose: To investigate the effect of trifolirhizin on neonatal rat model of asthma, and the mechanism of action involved.
Methods: Neonatal rats (n = 50) were randomly assigned to 5 groups (10 pups/group): sham, asthma and three treatment groups. With the exception of sham group, the rat pups were sensitized intraperitoneally with ovalbumin (OVA) at a dose of 20 µg/kg on days 7 and 21 postpartum. Rats in the treatment groups received trifolirhizin intragastrically at doses of 2, 4 and 5 mg/kg on day 7 postpartum. Eosinophils in bronchoalveolar lavage fluid (BALF) were counted using hematological analyzer. Serum immunoglobulin (Ig)E and interleukin (IL)-4, IL-5 and IL-13 levels in BALF were determined using their respective enzyme-linked immunosorbent assay (ELISA) kits. Messenger RNA (mRNA) expressions of mucin 5AC (Muc5AC), mucin 5B (Muc5B), tumor necrosis factor α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) were determined using immunohistochemical staining, while the protein expression of inhibitor of nuclear factor of kappa light polypeptide gene enhancer in B-cells alpha (IκBα) was assayed by Western blotting.
Results: Serum IgE level was significantly higher in asthma group than in sham group, but was significantly and dose-dependently reduced after treatment with trifolirhizin (p < 0.05). Lung tissue damage was also significantly mitigated in the treatment groups, relative to asthma group (p < 0.05). Trifolirhizin treatment significantly and dose-dependently downregulated the mRNA expressions of Muc5AC, Muc5B, TNF-α and ICAM-1, but upregulated IκBα protein expression significantly and dosedependently (p < 0.05). Bronchoalveolar lavage fluid (BALF) levels of IL-4, IL-5 and IL-13 were significantly higher in asthma group, but were significantly and dose-dependently reduced after treatment with trifolirhizin (p < 0.05).
Conclusion: These results indicate that trifolirhizin mitigates OVA-induced lung inflammation and tissue damage in neonatal rats via inhibition of NF-κB signaling pathway, thus affording a potential therapeutic strategy for the management of asthma
