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Systematic transcriptome and molecular docking analyses reveals that Cirsium japonicum mitigates allergic nasal inflammation through regulation of NRF2-mediated mucin production in an allergic rhinitis mouse model

ABSTRACT: Allergic rhinitis (AR) is a typical allergic disease mediated by immunoglobulin E (IgE), which greatly affects the quality of life and is more sensitive to change of seasons due to various nasal symptoms. AR worsening symptoms can lead to more dangerous diseases, there is an urgent need to develop safe and effective treatments. Cirsium japonicum (CSJ) is a plant that has been used in traditional medicine due to its various efficacy and safety; so far, the effects and major mechanisms of CSJ on AR have not been reported. Therefore, the purpose of this study was to investigate the possible targets of CSJ for AR treatment and its underlying mechanisms. An ovalbumin (OVA)-induced AR mouse model was established and the therapeutic effects of CSJ were evaluated. CSJ reduced the production level of OVA-specific IgE, histamine, and Th2 cytokines in serum, and significantly alleviated the typical symptoms of AR and the level of inflammation in the nasal mucosa. In addition, we used transcriptome analysis in AR models to identify that O-linked glycosylation of mucins, MUC5AC, and NRF2 are key targets for CSJ related to AR. Then, we identified the active ingredients of CSJ for AR, and verified that the active core compounds of CSJ, cryptochromogenic acid and cirsimarin, could bind closely to potential key targets, NRF2-KEAP1, and MUC5AC using molecular docking analysis. In conclusion, our results suggest that CSJ may be a more effective candidate drug for the treatment of AR with dual function to regulate both NRF2 pathway and MUC5AC expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE246623 | GEO | 2024/10/23

REPOSITORIES: GEO

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Project description:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ¬± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls. 38 samples classified in 4 categories : 14 isolated rhinitis (R), 6 rhinitis with uncontrolled asthma (UA), 7 rhinitis with controlled asthma (CA) and 11 healthy subjects (C )

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Systematic transcriptome and molecular docking analyses reveals that Cirsium japonicum mitigates allergic nasal inflammation through regulation of NRF2-mediated mucin production in an allergic rhinitis mouse model

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