Chrysin Ameliorates Ovalbumin‑Induced Allergic Response in Allergic Rhinitis: Potential Role of GATA‑3, T‑Box Protein Expressed in T Cells, Nuclear Factor‑Kappa B, and Nuclear Factor Erythroid 2‑Related Factor 2

Aim: This study aimed to determine the efficacy and mechanism of action of chrysin against allergic rhinitis (AR) induced by ovalbumin (OVA) in experimental mice. Materials and Methods: Induction of AR was performed in BALB/c mice via intraperitoneal administration sensitization and intranasal challenge with of OVA. Chrysin was concomitantly administered in mice at doses of 10, 20, and 40 mg/kg, p.o. Results: OVA challenge caused statistically significant (P < 0.05) increase in nasal rubbing, sneezing, and discharge as well as elevated serum histamine, β‑hexosaminidase, IgE (OVA‑specific and total) levels, whereas chrysin treatment at a dose of 20 and 40 mg/kg significantly (P < 0.05) inhibited these biomarkers and thus reduced nasal symptoms. The elevated total and differential cell count, splenic oxido‑nitrosative stress, and myeloperoxidase levels after OVA administration decreased statistically significantly (P < 0.05) by chrysin. There was a significant increase in the levels of tumor necrosis factor‑alpha (TNF‑α), interleukin (IL)‑4, IL‑1β, IL‑4/interferon‑gamma, IL‑6, and IL‑13 in nasal lavage fluid after OVA challenge, which was inhibited statistically significantly (P < 0.05) by chrysin. It also statistically significantly (P < 0.05) downregulated spleen GATA‑3 and nuclear factor‑kappa B (NF‑κB), whereas upregulated T‑box protein expressed in T cells (T‑bet) and nuclear factor erythroid 2‑related factor 2 (Nrf2) mRNA expression in spleen. Histological alteration induced in nasal and spleen tissue after OVA challenge was statistically significantly (P < 0.05) ameliorated by chrysin treatment. Conclusion: Chrysin modulated GATA‑3/T‑bet pathways and inhibited NF‑κB activation, thus attenuating the release of various inflammatory mediators (TNF‑α, IL‑1β, histamine, IgE, and β‑hexosaminidase), Th2 cytokines (ILs), and oxido‑nitrosative stress (Nrf2) to exert its anti‑allergic potential in experimental AR.