Ursolic Acid Alleviates Mucus Secretion and Tissue Remodeling in Rat Model of Allergic Rhinitis After PM2.5 Exposure

Author:

Sun Na1ORCID,Deng Congrui2,Zhao Qianbiao3,Han Zhijin1,Guo Zhiqiang1,Wang Hong1,Dong Weiyang2,Duan Yusen3,Zhuang Guoshun2,Zhang Ruxin1ORCID

Affiliation:

1. Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai, China

2. Center for Atmospheric Chemistry Study, Department of Environmental Science and Engineering, Fudan University, Shanghai, China

3. Shanghai Environmental Monitoring Center, Shanghai, China

Abstract

Background According to recent epidemiologic studies, exposure to fine particulate matter (particulate matter 2.5 ≤ µm [PM2.5]) in the air increases the incidence and severity of allergic rhinitis (AR). Ursolic acid (UA) has activities in immune regulation and anti-inflammatory. However, the role of UA intervention on PM2.5-exposed AR remains unknown. In this study, we investigated the effects of UA on tissue remodeling and mucus hypersecretion in a rat model of AR after PM2.5 exposure. Methods AR was induced in rats with ovalbumin (OVA) and they were exposed to ambient PM2.5(200 µg/m3) via a PM2.5 inhalation exposure system for 30 days(ARE group). Ursolic acid intervention was administrated in the AR model after PM2.5 exposure (UA group). Hyperplasia of goblet cells was detected by periodic acid-Schiff (PAS) staining and collagen deposition in the nasal mucosa was detected by Masson trichrome (MT) staining.MUC5AC expression was measured by immunohistochemistry. Results UA group showed reduced goblet cell hyperplasia and collagen deposition in the nasal mucosa which exacerbated after PM2.5 exposure, as reflected by PAS and MT staining when compared with the ARE group. Immunohistochemical results showed that the expression of MUC5AC in the UA group was lower than that in the ARE group. Conclusion Analysis of our data indicated that UA could attenuate nasal remodeling and mucus hypersecretion in aggravation of AR after PM2.5 exposure, which may be the pathophysiologic mechanisms for the prevention of AR exacerbated by exposure to PM2.5.

Funder

the National Natural Science Foundation of China

Publisher

SAGE Publications

Subject

General Medicine,Otorhinolaryngology,Immunology and Allergy

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