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Year : 2022  |  Volume : 18  |  Issue : 78  |  Page : 261-266

Anti-inflammatory and antiallergic activity of arbutin against ovalbumin-induced allergic rhinitis in mice through the modulation of inflammatory responses

1 Department of Otorhinolaryngology, Head and Neck Surgery, Yan'an University Affiliated Hospital, Yan'an, China
2 Department of Otorhinolaryngology Surgery, The Second Affiliated Hospital of Xi'an Medical University, Xi'an, China
3 Department of Otorhinolaryngology, Head and Neck Surgery, Xi'an Children's Hospital, Xi'an, China

Correspondence Address:
Ruiping Fang
Department of Otorhinolaryngology, Head and Neck Surgery, Xi'an Children's Hospital, Xi'an, 710 003
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_14_21

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Background: Allergic rhinitis (AR) is the prevalent inflammatory disease in the airway due to allergic reactions in response to numerous allergens. AR is considered as a type-I allergic condition and proceeded as early- and late-phase hypersensitivity. Objectives: In the existing work, we scheduled to discover the anti-inflammatory potential of arbutin against the ovalbumin (OVA)-provoked AR in mice through modulation of inflammation. Materials and Methods: The AR was triggered to the BALB/c mice by injecting 500 μL of OVA sensitization solution and then treated with the arbutin (25 and 50 mg/kg, respectively). Dexamethasone was used as standard. The occurrences of sneezing and nasal rubbing were detected within 15 min after the last OVA challenge. The status of OVA-specific immunoglobulin E (IgE), histamine, and malondialdehyde (MDA) was scrutinized by using assay kits. The status of NF-κB/IκBα and STAT-3 signaling molecules and its related cytokines was considered by using assay kits. The histological scores were evaluated by the histological alterations. Results: The arbutin supplementation lessened the incidence of nasal rubbings and sneezing, OVA-specific IgE and histamine, and MDA status. The arbutin-administered AR mice established the appreciable reduction in the NF-κBp65, phosphorylated IκBα, interleukin (IL)-1β, and tumor necrosis factor-α levels, also improved the IκBα status in the AR mice. Arbutin reduced the STAT-3, phosphorylated STAT-3, RORc, IL-17A, IL-5, and IL-6 levels and elevated the IL-10, IL-12, and IFN-γ status. Arbutin supplementation to the AR mice exhibited the considerable amelioration of the histological scores of OVA-provoked AR mice. Conclusion: Our results established that the arbutin treatment effectively ameliorated the OVA-provoked AR in mice through the modulation of inflammation, and it could be auspicious therapeutic agent to treat the RA.

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