HDAC inhibitor sodium butyrate prevents allergic rhinitis and alters lncRNA and mRNA expression profiles in the nasal mucosa of mice

• Published in: International journal of molecular medicine Vol. 45; no. 4; pp. 1150 - 1162
• Main Authors: Wang, Jie, Cui, Mu, Sun, Fei, Zhou, Ke, Fan, Bei, Qiu, Jian-Hua, Chen, Fu-Quan
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications UK Ltd 01.04.2020; D.A. Spandidos
• Subjects: Aluminum; Ethanol; Feeds; Gene expression; Laboratories; Nose; Pathogenesis; Proteins; Rhinitis; China
• ISSN: 1107-3756; 1791-244X
• DOI: 10.3892/ijmm.2020.4489

Our previous study demonstrated that intranasal administration of histone deacetylase inhibitor sodium butyrate (NaB) exhibits therapeutic effects on a mouse model of allergic rhinitis (AR). However, whether NaB is effective on AR when administered orally and prophylactically, as well as its potential effects on gene expression, remained unknown. The present study aimed to investigate the preventive effect of NaB on AR when added to the diet of newly weaned mice and to evaluate the changes in long non‑coding (lnc)RNA and mRNA expression profiles in the nasal mucosa. Mice were randomly divided into three groups as follows: i) Control (C) group, (no treatment); ii) AR group [treated with ovalbumin (OVA)]; and iii) NaB + AR group (treated with OVA and NaB). The NaB + AR group was administered NaB in their feed (30 g/kg chow), whereas the other two groups were fed normal feed between 3 and 6 weeks of age. At 7 weeks of age, OVA administration was initiated to induce AR in the AR and NaB + AR groups. Following model establishment, behavioral assessments, western blotting and gene expression analysis were performed. NaB exhibited a preventive effect in the murine AR model, diminished the increases in histone deacetylase 1 (HDAC1) and HDAC8 expression and increased OVA‑induced acetylation of histone H3 at lysine 9. In addition, NaB increased the AR‑associated low expression of interleukin 2 (IL‑2), interferon γ and IL‑17 and decreased the expression of IL‑4, IL‑5 and transforming growth factor β1. Gene Ontology and pathway analyses revealed the top 10 pathways among the groups. Octamer‑binding transcription factor 1, ecotropic viral integration site 1 and paired box 4 were predicted to be target genes of lncRNA (NONMMUT057309). Thus, NaB may exhibit a preventive effect on AR. Additionally, the lncRNA and mRNA expression profiles in the nasal mucosa of mice with AR differed significantly following NaB treatment. These results may provide insights into the pathogenesis of AR and suggest new treatment targets.