Background: Allergic rhinitis, a type 2 inflammatory sickness, is mediated by immunoglobulin E in nasal mucosa due to airborne allergens and formed inflammatory infiltrates containing of eosinophils, mast cells, basophils, and T-cells, which escorts the secretion of granule proteins, cytokines, and chemokines, thereby inducing the onset of clinical symptoms. Brucine, an indole alkaloid, it activates anti-inflammation, antitumor, antiproliferative property, and antiangiogenic in a tumor and it is considered for the usefulness in the cure of analgesia, diabetes, anemia, and gonorrhea. Contrariwise, the role of brucine on allergic rhinitis (AR) was unresolved. Materials and Methods: Hence, the vital mechanism indispensable for the defending achievement of brucine was discovered by giving ovalbumin (OVA) to mice. BALB/c mice were induced for AR by OVA administration. Brucine and dexamethasone were given before OVA. Nasal physical rubbing, the generation of cytokine response, and histological examination studies were achieved in mice. Results: Nasal rubbing and sneezing were enhanced in the brucine group of mice than in the AR group of mice. Above and beyond, the malondialdehyde level was diminished and prevented the signaling of cytosolic STAT3 and NF-kappa Bp65 pathway activation through the modulation of anti-inflammatory cytokines. Conclusion: Moreover, brucine abridged signs of augmented goblet cells, vascular congestions in the lamina, elevated ciliary loss, and improved eosinophil filtration in the AR model. Hence, our finding outcomes exposed that brucine has an auspicious tactic meant for immunotherapy in AR disease.