Date Published: June 11, 2018
Publisher: BioMed Central
Author(s): Jian Li, Bin Wang, Yingying Luo, Yajie Bian, Ruipei Wang.
Allergic rhinitis (AR), characterized by sneezing, nasal itching and rhinorrhea, affects a large number of population. This study aimed to explore the effects of artemisinin alone or combined with neurectomy of pterygoid canal in ovalbumin-induced AR mouse model and illustrate the underlying mechanisms.
Allergic symptoms were evaluated to verify inhibitory effect of artemisinin alone or combined with neurectomy of pterygoid canal on AR. Serum levels of histamine, immunoglobulin E (IgE) and inflammatory factors TNF, INF-γ, IL-1β IL-10, IL-4 and IL-5 were measured by ELISA. The mRNA levels of TNF, INF-γ, IL-1β and IL-10 in local lymph nodes were measured by RT-qPCR. The total and phosphorylated levels of ERK and JNK were assessed by Western blot. CD4+CD25+Foxp3+ T (Treg) cells were analyzed by flow cytometry.
Artemisinin significantly relieved the behavior symptoms of AR mice. The administration of artemisinin strikingly suppressed the expression of histamine, IgE and inflammatory factors. An increased Treg cell proportion and inhibited ERK phosphorylation were observed in artemisinin-treated groups as compared to those in the AR group. Moreover, artemisinin plus neurectomy of pterygoid almost abolished the behavioral score increase in AR mice.
These results indicated that artemisinin exhibited anti-allergic effect by inhibiting ERK activation and increasing Treg cell proportion, which subsequently decreased the expressions of allergic mediators. In addition, artemisinin combined with neurectomy of pterygoid showed better efficacy than artemisinin alone.
The online version of this article (10.1186/s13223-018-0249-6) contains supplementary material, which is available to authorized users.
Allergic rhinitis (AR), a nasal mucosal inflammation resulting from immunoglobulin E (IgE)-mediated hypersensitivity reaction, is characterized by sneezing, nasal itching, nasal obstruction, in any combination [1, 2]. AR has become a global health problem and affects a large number of population . Allergen exposures induce the recruitment of inflammatory cells, including eosinophils, basophils, mononuclear cells and mast cells, into the nasal mucosa. The activated inflammatory cells release several allergic mediators, such as histamine, leukotrienes and a number of cytokines and chemokines, to sustain inflammatory reactions and generate characteristic nasal symptoms . AR animal models have been studied to illustrate the underlying mechanisms leading to the generation of allergic inflammation and the efficacy of anti-allergic drugs. Repeated ovalbumin (OVA) exposure of mice has been used to establish an AR model with the infiltration of inflammatory cells and increased epithelial layer thickness .
Artemisinin, a sesquiterpene lactone, is isolated from the traditional Chinese herb Artemisia annua L. . It was discovered by Chinese scientist Tu Youyou, who has won the 2015 Nobel Prize in Medicine for her discovery. Artemisinin combination therapies (ACTs) are now standard treatment worldwide for malaria . Numerous studies have demonstrated the biological actions of artemisinin in various diseases [9–13]. Although artemisinin has anti-inflammatory effect, its anti-allergic activity has not been commonly reported yet. In the current study, we used a mouse model of AR to examine the effect of artemisinin intranasal instillation on allergic symptoms and explore the underlying mechanisms.
Our present study provides solid evidence that artemisinin exhibits anti-allergic roles by suppressing allergic responses in AR mouse model. The possible mechanism is that artemisinin treatment decreases expressions of allergic mediators in AR by inhibiting ERK activation and increasing Treg cell population. Moreover, artemisinin combined with neurectomy of pterygoid, a more promising strategy, exhibits better efficacy than artemisinin alone.