Allergic rhinitis is a sensitivity to allergens that causes swelling or puffiness of the nasal airways. The occurrence of allergic rhinitis is mounting worldwide. We examined whether fucoxanthin restrains the development of allergic rhinitis provoked by ovalbumin (OVA). In this study, allergic rhinitis in male BALB/c mice was induced with OVA. The object was to evaluate the effect of fucoxanthin on consequently allergic mice. Allergic responses like rubbing and sneezing were scored to reveal the effect of fucoxanthin in the induced and treated groups. Mean histological scores demonstrated variation in and between OVA-induced and fucoxanthin-treated groups in terms of ciliary loss, eosinophil infiltration, and the like. Lipid profiling (malondialdehyde) confirmed the restraining effect of fucoxanthin on allergic rhinitis. The present study showed that cytokine production, the induction of cell survival molecule NF-kappa B p65, and subsequent prevention of I kappa B alpha phosphorylation are controlled by fucoxanthin, and that interleukins (IL-5, IL-6, and 1L-12) support STAT-3 binding to key elements that control IL-17A expression. Additionally, the study showed that interleukin-induced NF-kappa B and I kappa B alpha directly regulate interleukins in collaboration with STAT-3 and related cytokines. Levels of IgE and histamine are the most frequent medications used to treat allergic rhinitis. Considering our findings, we concluded that fucoxanthin represses the development of allergic rhinitis induced by OVA and thus might be a positive drug for its management.