Apigenin Attenuates Allergic Responses of Ovalbumin-Induced Allergic Rhinitis Through Modulation of Th1/Th2 Responses in Experimental Mice

Abstract

Background: Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated immune-inflammatory response mainly affecting nasal mucosa. Apigenin, a flavonoid, has been documented to possess promising anti-allergic potential.Aim: To determine the potential mechanism of action of apigenin against ovalbumin (OVA)-induced AR by assessing various behavioral, biochemical, molecular, and ultrastructural modifications.Materials and Methods: Allergic rhinitis was induced in BALB/c mice (18-22 grams) by sensitizing it with OVA (5%, 500 mL, intraperitoneal [IP] on each consecutive day, for 13 days) followed by intranasal challenge with OVA (5%, 5 mL per nostril on day 21). Animals were treated with either vehicle (distilled water, 10 mg/kg, IP) or apigenin (5, 10, and 20 mg/kg, IP). Results: Intranasal challenge of OVA resulted in significant induction (P < .05) of AR reflected by an increase in nasal symptoms (sneezing, rubbing, and discharge), which were ameliorated significantly (P < .05) by apigenin (10 and 20 mg/kg) treatment. It also significantly inhibited (P < .05) OVA-induced elevated serum histamine, OVA-specific IgE, total IgE, and IgG1 and b-hexosaminidase levels. Ovalbumin-induced increased levels of interleukin (IL)-4, IL-5, IL-13, and interferon (IFN)-g in nasal lavage fluid were significantly decreased (P < .05) by apigenin. Ovalbumin-induced alterations in splenic GATA binding protein 3 (ie, erythroid transcription factor) (GATA3), T-box protein expressed in T cells (T-bet), signal transducer and activator of transcription-6 (STAT6), suppressor of cytokine signaling 1 (SOCS1), nuclear factor-kappa B (NF-kB), and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha messenger RNA, as well as protein expressions were significantly inhibited (P < .05) by apigenin. It also significantly ameliorated (P < .05) nasal and spleen histopathologic and ultrastructure aberration induced by OVA.Conclusion: Apigenin regulates Th1/Th2 balance via suppression in expressions of Th2 response (IgE, histamine, ILs, GATA3, STAT6, SOCS1, and NF-kB) and activation of Th1 response (IFN-g and T-bet) to exert its anti-allergic potential in a murine model of OVA-induced AR.

Ajwain oil attenuates allergic response of ovalbumin‐induced allergic rhinitis via alteration of inflammatory, oxidative stress, and Th1/Th2 responses

“…Ajwain oil significantly suppressed the incidence of nose scratching and sneezing, especially the higher dose of Ajwain oil exhibited the beneficial effect. Compared with the standard group, the Ajwain oil group rats had a significant beneficial effect (after 28 days of administration), which corresponds to the previous research (Chen, He, et al., 2020). The result suggests that the Ajwain oil having protective effect against AR by reducing the nasal‐allergic symptoms in rats.…”

Chlorogenic acid ameliorated allergic rhinitis-related symptoms in mice by regulating Th17 cells

“…The pathogenesis of AR is generally accepted as imbalanced T helper cells (Th) 1/Th2 immunological reaction mechanism [ 5 , 6 ]. Th1 and Th2, two subsets of helper T cells with different functions are important in regulating immune response [ 7 , 8 ].…”

Pharmacological Effects of Polyphenol Phytochemicals on the JAK-STAT Signaling Pathway

“…Programmed death in colon cancer cells can be induced by inhibition of STAT3 phosphorylation, thereby downregulating the antiapoptotic proteins Bcl-XL and Mcl-1 (Maeda et al, 2018). Apigenin can suppress the levels of IL-4, IL-5, IL-13, and IFN-g in Ovalbumin-Induced Allergic Rhinitis mouses Nasal lavage fluid (NLF) and inhibit the expression of p-STAT6 and SOCS1 (Chen et al, 2020).…”