Abstract
Abstract Allergic rhinitis (AR) is a serious health concern across the globe. Despite its non-fatal character, it accounts for affecting millions of people across the world and is deemed responsible to affect their quality of life and put a significant economic burden. In the current study, we aimed to assess the anti-allergic and anti-inflammatory effects and the underlying molecular mechanisms of ellipticine (ETC) against AR using ovalbumin (OVA)-induced murine model of allergic rhinitis. The ETC was administered to mice via intra-peritoneal route after suspending in 5% CMC after sensitization by OVA. Results of the study suggested that ETC causes a significant reduction the nose rubs as compared to disease control. A significant reduction in the serum level of histamine, IgG1, TNF-α, IL-1β, MIP-2, and IL-6 was found in ETC treated group in a dose-dependent manner as compared to OVA challenged mice. It also reduces eosinophils in BALF of AR mice. In western blot analysis, the expression of aberrantly activated COX-2 and NF-ĸB found significantly reduced in ETC treated group due to inhibition of TLR-4 and caspase-1 as compared to disease-control mice. ETC showed significant interaction with residues of the active site of COX-2 and NF-ĸB. Collectively, our results indicated that ETC can be used to improve present therapeutic strategies against AR.
Highlights
Allergic rhinitis is a serious global health concern affecting mucosal tissue of the nasal cavity
The serum level of histamine was found significantly upregulated in OVA mice as compared to control, which was reduced significantly upon administration of ETC, Fig 1B
The effect of ETC was determined on the serum levels of immunoglobulins, such as, immunoglobulins E (IgE), IgG1, and IgG2a which play a key role in mediating immune response against Allergic rhinitis (AR)
Summary
Allergic rhinitis is a serious global health concern affecting mucosal tissue of the nasal cavity. The AR is caused due to allergens, which are responsible for the induction of hypersensitivity reaction in the affected individuals. To induce a cascade of inflammatory reactions mediated via immunoglobulins E (IgE) like antibodies (Incorvaia et al, 2018; Small et al, 2018). The clinical symptoms of AR include sneezing, rhinorrhea, itching induced due to acute activation and infiltration of inflammatory cells, which include, mast cells, eosinophils, and other types. These inflammatory cells upon recruitment lead to the production of various inflammatory mediators such as histamine, serotonin, nucleotides, proteases, and tumor necrosis factor (TNF)-α. The nasal mucosa is the primary site for allergen exposure and the inflammatory reactions that cause AR symptoms. The mechanisms driving AR pathophysiology are multifaceted and include activation and migration of effector cells, the release of mediators, chemokines, and cytokines from inflammatory cells, and damage to the nasal epithelium and nerve endings (Amin, 2012; Zissler et al, 2016)
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