Apigenin attenuates inflammatory response in allergic rhinitis mice by inhibiting the TLR4/MyD88/NF‐κB signaling pathway

Abstract

Background: Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated immune inflammatory response that mainly affects the nasal mucosa. Currently, there is evidence that apigenin, as a flavonoid, has anti-allergic potential. Material/Methods: In vitro, compound 48/80 and lipopolysaccharide (LPS) were used to induce mast cell activation and inflammation in HMC-1 cells. In vivo, ovalbumin (OVA) induced and stimulated AR in BALB/c mice. ELISA was used to detect the contents of β-hexosaminidase, histamine, eosinophil cationic protein (ECP), OVAspecific IgE, IgG1, and IgG2a, inflammatory factors in cells and mouse serum. Cell viability and apoptosis were measured with MTT and flow cytometry. Toll like receptor 4 (TLR4)/myeloid differentiation factor88 (MyD88)/Nuclear transcription factor-κB (NF-κB) pathway-related proteins in cells and mouse nasal mucosa tissues were analyzed with Western blotting. The levels of Th1 (IFN-γ) and Th2 (IL-4, IL-5, and IL-13) cytokines and Th1 (T-bet) and Th2 (GATA-3) specific transcription factors were also assessed. The ratio of Th1 (CD4 + IFN-γ + ) / Th2 (CD4 + IL-4 + ) cells in mouse peripheral blood mononuclear cells was evaluated by flow cytometry. Results: Apigenin significantly inhibited compound 48/80-induced secretion of β-hexosaminidase and histamine. Apigenin blocked LPS-induced decrease in cell viability and increase in cell apoptosis and inflammatory cytokine secretion by suppressing the activity of the TLR4/MyD88/NF-κB pathway. Apigenin treatment reduced the levels of OVA-specific IgE, IgG1 and IgG2a as well as β-hexosaminidase, histamine and ECP levels in mouse serum. Moreover, administration with apigenin decreased Th2 cytokine and transcription factor levels and increased Th1 cytokine and transcription factor levels, and promoted the ratio of Th1/Th2 cells in AR mice. Additionally, apigenin significantly alleviated nasal symptoms and nasal eosinophil infiltration in AR mice. Conclusions: Apigenin alleviates the inflammatory response of allergic rhinitis by inhibiting the activity of the TLR4/MyD88/NF-κB signaling pathway.

Cang-ai volatile oil alleviates nasal inflammation via Th1/Th2 cell imbalance regulation in a rat model of ovalbumin-induced allergic rhinitis

“…In AR, histamine plays an important part in itching, sneezing, and nasal congestion ( Yokota et al, 2015 ). After allergen excitation in the nose, the histamine level is increased in the nasal lavage of allergic individuals compared with that of non-allergic individuals ( Li et al, 2023 ). CAVO lowered the serum histamine level in rats with OVA-induced AR, alike that seen with the positive control (loratadine).…”

Apigenin: A Bioflavonoid with a Promising Role in Disease Prevention and Treatment

“…Apigenin meaningfully suppressed the production of these inflammatory cytokines compared to the LPS group [ 52 ]. A study result demonstrated that administration with apigenin increased Th1 cytokine and transcription factor levels and decreased Th2 cytokine and transcription factor levels and promoted the ratio of Th1/Th2 cells in allergic rhinitis mice [ 53 ]. The objective of the study was to investigate the anti-inflammatory effects of apigenin to evaluate its potential as an anti-psoriatic agent.…”

Tolerogenic dendritic cells and TLR4/IRAK4/NF-κB signaling pathway in allergic rhinitis

“…Li et al. ( 112 ) showed that apigenin could attenuate the inflammatory response in AR through the TLR4/MyD88/NF-κB signaling pathway. Liu et al.…”