Chen Jinwei, Zhou Yongling
Am J Vet Res. 2024 May 6;85(6). doi: 10.2460/ajvr.24.02.0031. Print 2024 Jun 1.
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.
126 BALB/c mice.
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.
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.
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.
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。
126只BALB/c小鼠。
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。
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。
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。
