Kirenol ameliorated ovalbumin-induced allergic rhinitis in mice via suppression of oxidative stress and inflammatory response

Abstract

Background: Allergic rhinitis (AR) is a type-1 inflammatory ailment characterized by the recurrent nasal rubbings, sneezing, and other unpleasant symptoms. AR is an imperative airway inflammatory ailment that affects nearly 20%–30% of the global population. Kirenol is a bioactive diterpenoid with numerous beneficial properties. Objectives: In this study, we aimed to assess the therapeutic role of kirenol against the ovalbumin (OVA)-induced AR in mice via suppression of oxidative and inflammatory responses. Materials and Methods: AR was induced in BALB/c mice via administration of OVA. Subsequently, the animals were administered with 20 and 30 mg/kg of kirenol. Dexamethasone was utilized as the standard drug. The frequencies of nasal rubbings and sneezing of the mice were recorded. The status of histamine, OVA-specific immunoglobulin E (IgE), prostaglandin-D2 (PGD2), and leukotriene C4 (LTC4) was examined by using commercial assay kits. The levels of eosinophil cationic protein (ECP), interleukin (IL)-4, IL-5, IL-6, IL-33, and tumor necrosis factor (TNF)-α were investigated through the marker-specific assay kits. The mononuclear cells were isolated from the spleen of the animals of untreated AR group and cultured in an RPMI-1640 medium. The mRNA expression of a thioredoxin-interacting protein (TXNIP) in the spleen cells was studied by real-time polymerase chain reaction technique. The status of oxidative stress and inflammatory cytokines was examined by using assay kits. Results: Kirenol (20 and 30 mg/kg)-administered AR mice exhibited reduced frequency of nasal rubbing and sneezing. Kirenol effectively reduced the status of OVA-specific IgE and histamine in AR mice. The status of PGD2, LTC4, IL-4, IL-5, IL-6, IL-33, TNF-α, ECP status, and eosinophil count was diminished by the kirenol. The level of malondialdehyde and reactive oxygen species was reduced and the activity of superoxide dismutase markedly was improved by the kirenol. The kirenol-supplemented spleen-derived mononuclear cells showed downregulation of mRNA expression of TXNIP. Conclusion: These results demonstrate the curative role of kirenol against the OVA-mediated AR in mice, which can be a promising agent to treat AR in humans in future.