Coptisine Suppresses Mast Cell Degranulation and Ovalbumin-Induced Allergic Rhinitis.

Shuilian Fu,Tie Hong,Danni Wang,Saihong Ni

doi:10.3390/molecules23113039

Abstract

Coptisine is one of the main components of isoquinoline alkaloids in the coptidis rhizome. The effect of coptisine on allergic rhinitis has not been investigated. In this study, we report the effects and mechanisms of coptisine using monoclonal anti-2,4,6-dinitrophenyl-immunoglobulin (Ig) E/human serum albumin (DNP-IgE/HSA)-stimulated rat basophilic leukemia cells (RBL-2H3 cells) in vitro and an ovalbumin (OVA)-induced allergic rhinitis (AR) in mice. The results showed that coptisine markedly decreased the levels of β-hexosaminidase, histamine, interleukin (IL)-4, and tumor necrosis factor (TNF)-α. Coptisine also prevented morphological changes, such as restoring an elongated shape, inhibiting granule release on toluidine blue staining, and reorganizing inhibited filamentous actins (F-actin). Additionally, coptisine blocked the phosphorylation of phosphoinositide3-kinase (PI3K)/Akt (as known as protein kinase B(PKB)) in RBL-2H3 cell. Furthermore, the results showed that coptisine suppressed OVA-induced allergic rhinitis symptoms, such as nasal rubbing and OVA-specific IgE, and histamine, IL-4 and TNF-α levels in the serum of AR mice. These data suggested that coptisine should have inhibitory effects on the inflammatory responses of mast cells, and may be beneficial for the development of coptisine as a potential anti-allergic drug.

Highlights

Allergic rhinitis (AR) is one of the most common allergic inflammatory diseases that effects millions of people worldwide; it is relevant to increased levels of allergen-specific immunoglobulin E (IgE), and derives from the sensitization of nasal mucosa with specific allergens including domestic dust mites, pets, and pollens [1,2]
The effects coptisine viability were studied ensure that decreased levels of mast cell granule were not due to the cell death
In IgE-mediated mast cell activation, the cells begin to product cytoplasmic granules with proinflammatory and pro-allergic mediators, which are released into the surrounding environment [27]

Summary

Introduction

Allergic rhinitis (AR) is one of the most common allergic inflammatory diseases that effects millions of people worldwide; it is relevant to increased levels of allergen-specific IgE, and derives from the sensitization of nasal mucosa with specific allergens including domestic dust mites, pets, and pollens [1,2] Clinical symptoms such as nasal rubbing, sneezing, nasal congestion, and obstruction seriously affect patient quality of life [3,4]. Mast cells are activated by cross-linking immunoglobulin E (IgE) binding to high-affinity IgE receptors (FcεRI) on their surface, which can bind IgE and induce mast cell degranulation following repeated-allergen stimulation [6]. During mast cell degranulation process, FcεRI-dependent signaling pathways such as phosphoinositide3-kinase (PI3K)

Methods

Results

Conclusion