Li Rong,
Pan Lei,
Li Yi,
Wu Yupei,
Gong Rui,
Liu Xin,
Xie Huimin,
Huang Qing
Department of Pediatrics, Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, China;
For correspondence:- Huang Qing
Email: ukhmfh@163.com Tel:+862782811080
Accepted: 16 October 2020
Published: 30 November 2020
Citation:
Rong L, Lei P, Yi L, Yupei W, Rui G, Xin L, et al.
Trifolirhizin mitigates ovalbumin-induced lung inflammation and tissue damage in neonatal rats via inhibition of the NF-κB signaling pathway. Trop J Pharm Res 2020; 19(11):2303-2308
doi:
10.4314/tjpr.v19i11.8
© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
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 dose-dependently (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.
Keywords: Asthma, Bronchoalveolar lavage fluid, Inflammation, Interleukins, Ovalbumin