BACKGROUND Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated immune-inflammatory response mainly affecting nasal mucosa. Apigenin, a flavonoid, has been documented to possess promising anti-allergic potential. AIM To determine the potential mechanism of action of apigenin against ovalbumin (OVA)-induced AR by assessing various behavioral, biochemical, molecular, and ultrastructural modifications. MATERIALS AND METHODS Allergic rhinitis was induced in BALB/c mice (18-22 grams) by sensitizing it with OVA (5%, 500 μL, intraperitoneal [IP] on each consecutive day, for 13 days) followed by intranasal challenge with OVA (5%, 5 μL per nostril on day 21). Animals were treated with either vehicle (distilled water, 10 mg/kg, IP) or apigenin (5, 10, and 20 mg/kg, IP). RESULTS Intranasal challenge of OVA resulted in significant induction (P < .05) of AR reflected by an increase in nasal symptoms (sneezing, rubbing, and discharge), which were ameliorated significantly (P < .05) by apigenin (10 and 20 mg/kg) treatment. It also significantly inhibited (P < .05) OVA-induced elevated serum histamine, OVA-specific IgE, total IgE, and IgG1 and β-hexosaminidase levels. Ovalbumin-induced increased levels of interleukin (IL)-4, IL-5, IL-13, and interferon (IFN)-γ in nasal lavage fluid were significantly decreased (P < .05) by apigenin. Ovalbumin-induced alterations in splenic GATA binding protein 3 (ie, erythroid transcription factor) (GATA3), T-box protein expressed in T cells (T-bet), signal transducer and activator of transcription-6 (STAT6), suppressor of cytokine signaling 1 (SOCS1), nuclear factor-kappa B (NF-κB), and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha messenger RNA, as well as protein expressions were significantly inhibited (P < .05) by apigenin. It also significantly ameliorated (P < .05) nasal and spleen histopathologic and ultrastructure aberration induced by OVA. CONCLUSION Apigenin regulates Th1/Th2 balance via suppression in expressions of Th2 response (IgE, histamine, ILs, GATA3, STAT6, SOCS1, and NF-κB) and activation of Th1 response (IFN-γ and T-bet) to exert its anti-allergic potential in a murine model of OVA-induced AR.

中文翻译：

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芹菜素通过调节实验小鼠的 Th1/Th2 反应来减轻卵清蛋白诱导的过敏性鼻炎的过敏反应。

背景变应性鼻炎（AR）是一种免疫球蛋白E（IgE）介导的免疫炎症反应，主要影响鼻粘膜。芹菜素是一种黄酮类化合物，已被证明具有良好的抗过敏潜力。目的通过评估各种行为、生化、分子和超微结构修饰来确定芹菜素对抗卵清蛋白 (OVA) 诱导的 AR 的潜在作用机制。材料和方法 在 BALB/c 小鼠（18-22 克）中诱导过敏性鼻炎，方法是用 OVA（5%，500 μL，每天腹膜内 [IP]，持续 13 天）致敏，然后用 OVA 鼻内攻击（ 5%，第 21 天每个鼻孔 5 μL）。用载体（蒸馏水，10 mg/kg，IP）或芹菜素（5、10 和 20 mg/kg，IP）处理动物。结果 OVA 的鼻内攻击导致显着诱导（P < 鼻部症状（打喷嚏、摩擦和分泌物）的增加反映了 AR 的 0.05），而芹菜素（10 和 20 mg/kg）治疗显着改善了（P < .05）。它还显着抑制 (P < .05) OVA 诱导的升高的血清组胺、OVA 特异性 IgE、总 IgE 以及 IgG1 和 β-氨基己糖苷酶水平。卵清蛋白诱导的鼻腔灌洗液中白细胞介素 (IL)-4、IL-5、IL-13 和干扰素 (IFN)-γ 水平的升高被芹菜素显着降低 (P < .05)。卵清蛋白诱导的脾脏 GATA 结合蛋白 3（即红系转录因子）（GATA3）、T 细胞中表达的 T-box 蛋白（T-bet）、信号转导和转录激活因子 6（STAT6）、细胞因子抑制因子的改变信号 1 (SOCS1)、核因子-kappa B (NF-κB)、芹菜素显着抑制B细胞抑制剂-α信使RNA中kappa轻多肽基因增强子的核因子和蛋白质表达（P < .05）。它还显着改善了 (P < .05) OVA 引起的鼻和脾组织病理学和超微结构畸变。结论 芹菜素通过抑制 Th2 反应（IgE、组胺、ILs、GATA3、STAT6、SOCS1 和 NF-κB）的表达和激活 Th1 反应（IFN-γ 和 T-bet）来发挥其抗-OVA诱导的AR小鼠模型中的过敏潜力。