Theabrownin attenuates OVA-induced allergic rhinitis by restoring lipid metabolism homeostasis and suppressing PPAR signaling pathway

Introduction Allergic rhinitis is a common type 2 immune-mediated inflammatory disease, with lipid metabolism disorder being one of its pathological features. Theabrownin, a bioactive component derived from tea, possesses anti-inflammatory and metabolic regulatory properties; however, its role in allergic rhinitis and the underlying mechanisms remain unclear. Methods The therapeutic potential of theabrownin against allergic rhinitis was evaluated using a murine model of OVA-induced AR. Nasal symptoms and pathological changes were assessed. Multiplex cytokine assay and untargeted serum metabolomics were performed to quantify inflammatory cytokines and lipid metabolites. In vitro, THP-1 macrophages were stimulated with OVA to induce M2 polarization, followed by theabrownin treatment. Transcriptome sequencing, WB, IF, and qRT-PCR were applied to investigate molecular mechanisms. Results Theabrownin significantly alleviated nasal symptoms and pathological changes in AR mice, downregulated serum levels of TNF-α, IL-13, IL-10, IL-5, and MCP-1. Untargeted metabolomics revealed that theabrownin ameliorated glycerophospholipid and cholesterol metabolism disorders. In vitro, theabrownin reversed OVA-induced M2 polarization of THP-1 cells, reducing the expression of M2 marker molecules (CD209, ALOX15, and PPARγ). KEGG enrichment analysis identified the PPAR signaling pathway as a potential key mediator, and subsequent WB, IF, and qRT-PCR confirmed that theabrownin suppressed activation of this pathway. Conclusions Theabrownin alleviates OVA-induced AR in mice by exerting anti-inflammatory effects and correcting lipid metabolism disorders, likely through modulation of the PPAR pathway. Our findings suggest that theabrownin is a promising immunometabolic regulator for AR treatment.