LAUSR

OBJECTIVE Luteolin (LO) has been reported to be a potential drug for allergic rhinitis (AR). This paper explored the mechanism of LO in AR. MATERIALS AND METHODS Mice were treated with ovalbumin (OVA) to construct an AR model in vivo before LO or 3-methyladenine (3-MA) treatment. The frequency of nasal sneezing was counted. The nasal mucosa thickness was assessed by hematoxylin-eosin staining assay. The levels of anti-OVA-immunoglobulin E (IgE)/IgG2a, autophagy-related factors (Beclin1, LC3II/LC3I), and T helper cell 17 (Th17)/regulatory T cell (Treg) markers (interleukin (IL)-17A, retinoic acid receptor-related orphan nuclear receptor γt (RORγt)/IL-10, forkhead box P3 (Foxp3)) were detected through enzyme-linked immunosorbent assay, western blot, and quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Flow cytometry assay was performed to test the percentage of Th17 and Treg cells. RESULTS The nasal sneezing frequency, nasal mucosa thickness, and levels of anti-OVA-IgE, Beclin1, LC3II/LC3I, IL-17A as well as RORγt were enhanced whereas anti-OVA-IgG2a, IL-10, and Foxp3 levels were inhibited in a mouse model of OVA-induced AR, which were reversed by LO or 3-MA treatment. CONCLUSIONS LO restored Treg/Th17 balance to ameliorate AR in a mouse model.