Effects of Ursolic Acid on the Expression of Th1–Th2-related Cytokines in a Rat Model of Allergic Rhinitis After PM2.5 Exposure

Na Sun, Zhijin Han, Hong Wang, Zhiqiang Guo, Congrui Deng, Weiyang Dong, Guoshun Zhuang, Ruxin Zhang

American Journal of Rhinology and Allergy · 2020 · 21 citations · 15 references

Concepts

Abstract

BACKGROUND: Allergic rhinitis (AR) is a global health problem and closely related to environmental factors. Ursolic acid (UA) has potential in the treatment of allergic inflammation. The effects of UA intervention on PM2.5-induced AR remain uncertain. OBJECTIVE: To assess the effects of UA on nasal symptoms and the expression of T-helper (Th)1-Th2-related cytokines in a rat model of AR after fine particulate matter (particulate matter ≤ 2.5 µm [PM2.5]) exposure. METHODS: PM2.5 for 30 days via inhalation (ARE group), and a group with UA intervention to the AR model after PM2.5 exposure (UA group). UA intervention was adopted after PM2.5 exposure in the UA group. Nasal symptoms and levels of Th1-Th2 cytokines in the serum were detected in each individual rat. The pathological changes and expression of Eotaxin in the nasal mucosa of each individual rat were examined by histology. RESULTS: PM2.5 significantly increased the number of sneezes and nasal rubs in the rats with AR, and UA alleviated these symptoms. UA decreased interleukin (IL)-4, IL-5, IL-13, Eotaxin-1, and OVA Immunoglobulin E (IgE) protein levels. In the AR group, hematoxylin and eosin staining showed disordered arrangement of the nasal mucosa epithelium, cell shedding, eosinophilic infiltration, swelling of the glands, and submucosal vascular congestion. UA group showed reduced eosinophilic infiltration and orderly arrangement of the mucosal epithelium when compared with the ARE group. Immunohistochemical results showed that the expression of Eotaxin in the UA group was lower than that in the ARE group. CONCLUSION: UA could relieve nasal symptoms caused by PM2.5 exposure, the possible mechanism of which is to inhibit the expression of Th2 cytokines, eosinophilic infiltration, and specific IgE production.

References

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