Chen Jinwei, Zhou Yongling
Am J Vet Res. 2024 May 6;85(6). doi: 10.2460/ajvr.24.02.0031. Print 2024 Jun 1.
OBJECTIVE: To examine the potential of galangin in a mouse model of ovalbumin (OVA)-induced allergic rhinitis (AR), as chronic AR, induced by immunoglobulin-E (IgE), leads to histamine release and nasal inflammation, and although galangin exhibits antiasthmatic and anti-inflammatory potential, its effect on AR is yet to be investigated. ANIMALS: 126 BALB/c mice. METHODS: AR induction involved sensitizing female mice with OVA (5%, 500 µL, IP) for 14 days. Post OVA challenge, the mice were divided into 7 groups (n = 18/group), including normal, AR control, montelukast (10 mg/kg), galangin (5, 10, and 20 mg/kg), and per se (galangin [20 mg/kg] treatment. Various outcomes were evaluated, including nasal symptoms, histopathology, biochemistry, and nasal lavage fluid inflammatory cytokines and signaling pathways in nasal mucosal to assess galangin potential in AR. RESULTS: In AR mice, galangin (10 and 20 mg/kg) significantly (P < .05) reduced sneezing, rubbing, and nasal discharge post-OVA challenge. Galangin treatment attenuated (P < .05) elevated serum histamine, β-hexosaminidase, IgE, and Immunoglobulin G1 levels in AR control mice. Additionally, galangin significantly (P < .05) decreased OVA-induced alterations in IL-4, IL-6, IL-13, and interferon-γ levels in nasal lavage fluid compared to AR control mice. Western blot analysis demonstrated that galangin lowered OVA-induced AR by significantly (P < .05) downregulating the phosphorylated protein kinase B and mammalian target of rapamycin-protein expressions while markedly (P < .05) upregulating the glycogen synthase kinase-3β protein expressions in nasal mucosal. Galangin also significantly ameliorated (P < .05) the OVA-induced histological aberrations in the nasal mucosa, reflected by reduced eosinophil infiltration, hyperplasia, and edema. CLINICAL RELEVANCE: Galangin exhibits antihistaminic and anti-inflammatory effects in AR mice by regulating IgE-mediated histamine and inflammatory release and modulating the phosphatidylinositol 3-kinase/Ak strain transforming/mammalian target of rapamycin pathways.
目的：在卵清蛋白（OVA）诱导的变应性鼻炎（AR）小鼠模型中研究高良姜素的作用，由于免疫球蛋白E（IgE）诱导的慢性AR会导致组胺释放和鼻黏膜炎症，尽管高良姜素具有抗哮喘和抗炎潜力，但其对AR的影响尚待研究。 动物：126只BALB/c小鼠。 方法：通过用OVA（5%，500μL，腹腔注射）致敏雌性小鼠14天来诱导AR。OVA激发后，将小鼠分为7组（每组n = 18），包括正常组、AR对照组、孟鲁司特（10mg/kg）组、高良姜素（5、10和20mg/kg）组以及高良姜素自身对照组（高良姜素[20mg/kg]处理）。评估了各种结果，包括鼻症状、组织病理学、生物化学以及鼻灌洗液中的炎性细胞因子和鼻黏膜中的信号通路，以评估高良姜素在AR中的潜力。 结果：在AR小鼠中，高良姜素（10和20mg/kg）在OVA激发后显著（P < 0.05）减少了打喷嚏、蹭鼻和鼻分泌物。高良姜素治疗使AR对照小鼠中升高的血清组胺、β-己糖胺酶、IgE和免疫球蛋白G1水平降低（P < 0.05）。此外，与AR对照小鼠相比，高良姜素显著（P < 0.05）降低了OVA诱导的鼻灌洗液中IL-4、IL-6、IL-13和干扰素-γ水平的变化。蛋白质免疫印迹分析表明，高良姜素通过显著（P < 0.05）下调磷酸化蛋白激酶B和雷帕霉素哺乳动物靶点蛋白的表达，同时显著（P < 0.05）上调鼻黏膜中糖原合酶激酶-3β蛋白的表达，从而降低OVA诱导的AR。高良姜素还显著改善（P < 0.05）了OVA诱导的鼻黏膜组织学异常，表现为嗜酸性粒细胞浸润、增生和水肿减少。 临床意义：高良姜素通过调节IgE介导的组胺和炎症释放以及调节磷脂酰肌醇3激酶/Akt丝氨酸/苏氨酸激酶/雷帕霉素哺乳动物靶点通路，在AR小鼠中表现出抗组胺和抗炎作用。
Eur Arch Otorhinolaryngol. 2023-2
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