Department of Otolaryngology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China (mainland).
Med Sci Monit. 2020 Sep 1;26:e923358. doi: 10.12659/MSM.923358.
BACKGROUND Allergic rhinitis (AR) is a prevalent atopic disorder caused by immune imbalance. Chlorogenic acid (CGA) has antibacterial, antiviral, antioxidative and immunoregulatory effects, but its role in anaphylactic disease remains unclear. The current study aimed to investigate the function of CGA in AR. MATERIAL AND METHODS AR mice models were induced with ovalbumin (OVA) by orally administrating the mice with 50 mg/kg (L-CGA), 100 mg/kg (M-CGA), or 200 mg/kg (H-CGA) of CGA. The number of nasal rubbings and sneezes was recorded. Afterward, the mice were sacrificed for the collection of blood, nasal lavage fluid (NALF), and nasal tissues. The cells in NALF were counted by hemocytometer and stained by Diff-Quick. Nasal mucosa was observed by H&E staining. ELISA testing was conducted for detecting the levels of anti-OVA antibodies and Th1/Th2-related cytokine. Quantitative real-time polymerase chain reaction experiments were conducted to determine mRNA expressions of Th1/Th2-related cytokines. RESULTS In the OVA-induced AR mice, CGA treatment reduced nasal rubbing and sneezing, and also suppressed the number of total cells, eosinophils, neutrophils, lymphocytes, macrophages, and epithelial cells in NALF. OVA-induced up-regulation of nasal mucosa thickness was inhibited by CGA, and the effects of OVA on IgE, IgG1, and IgG2a were reversed by CGA. The regulatory effects of OVA on mRNA expressions and levels of Th1/Th2-related cytokines were abolished by CGA treatment in AR mice. CONCLUSIONS CGA can alleviate allergic inflammatory responses through regulating Th1/Th2 balance in OVA-induced allergic rhinitis mice.
变应性鼻炎（AR）是一种由免疫失衡引起的常见特应性疾病。绿原酸（CGA）具有抗菌、抗病毒、抗氧化和免疫调节作用，但它在过敏疾病中的作用尚不清楚。本研究旨在探讨 CGA 在 AR 中的作用。
通过口服给予小鼠 50mg/kg（L-CGA）、100mg/kg（M-CGA）或 200mg/kg（H-CGA）的 CGA，诱导 AR 小鼠模型。记录鼻擦和打喷嚏的次数。然后处死小鼠，收集血液、鼻洗液（NALF）和鼻组织。用血细胞计数器计数 NALF 中的细胞，并通过 Diff-Quick 染色。用 H&E 染色观察鼻黏膜。通过 ELISA 检测检测抗 OVA 抗体和 Th1/Th2 相关细胞因子的水平。通过定量实时聚合酶链反应实验检测 Th1/Th2 相关细胞因子的 mRNA 表达。
在 OVA 诱导的 AR 小鼠中，CGA 治疗减少了鼻擦和打喷嚏次数，并抑制了 NALF 中总细胞、嗜酸性粒细胞、中性粒细胞、淋巴细胞、巨噬细胞和上皮细胞的数量。CGA 抑制了 OVA 诱导的鼻黏膜厚度增加，并逆转了 CGA 对 IgE、IgG1 和 IgG2a 的作用。CGA 治疗消除了 OVA 对 AR 小鼠 Th1/Th2 相关细胞因子 mRNA 表达和水平的调节作用。
CGA 通过调节 OVA 诱导的过敏性鼻炎小鼠的 Th1/Th2 平衡，可减轻过敏炎症反应。
