She N N, Hou Y, Wang Y H, Gui Y, Xi G H, Chen X W, Chen K B, Ma C X, Liu X H, Zhang X B
Department of Otolaryngology Head and Neck Surgery, the First Hospital of Lanzhou University, Lanzhou, 730000, China.
Lanzhou University.
Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2019 Mar;33(3):262-266. doi: 10.13201/j.issn.1001-1781.2019.03.019.
To observe the effect of 18β-sodium glycyrrhetinic acid(18β-SGA) on the expression of TNF-α in nasal mucosa of rats with allergic rhinitis（AR）, and explore the intervention mechanism of 18β-SGA on AR. One hundred and six SPF-level Wistar rats were randomly divided into control group, AR group, budesonide group, 18β-SGA low dose group and high dose group. After the AR rat model was constructed by ovalbumin, the rats were given drug intervention and sacrificed after 2 and 4 weeks of intervention. The nasal mucosa of the rats was taken for immunohistochemical staining, RT-qPCR and Western-blotting to localize and quantify the expression of TNF-α. By immunohistochemistry, Western-blotting and RT-PCR, TNF-α was mainly found in the columnar epithelium, vascular endothelium, glandular and some inflammatory cytoplasm of nasal mucosa. And the expression of TNF-α in the nasal mucosa of AR rats was significantly increased than the normal group at the protein and mRNA levels (<0.01). After intervention with different doses of 18β-SGA, the expression of TNF-α was significantly decreased (<0.01), especially after 4 weeks of 18β-SGA low dose group(<0.01). Different doses of 18β-SGA have therapeutic effects on AR, and its mechanism of action may be related to the inhibition of TNF-α expression.
观察18β-甘草次酸钠（18β-SGA）对变应性鼻炎（AR）大鼠鼻黏膜肿瘤坏死因子-α（TNF-α）表达的影响，探讨18β-SGA对AR的干预机制。将106只SPF级Wistar大鼠随机分为对照组、AR组、布地奈德组、18β-SGA低剂量组和高剂量组。用卵清蛋白构建AR大鼠模型后，对大鼠进行药物干预，干预2周和4周后处死。取大鼠鼻黏膜进行免疫组织化学染色、RT-qPCR和Western印迹法，对TNF-α的表达进行定位和定量分析。通过免疫组织化学、Western印迹法和RT-PCR发现，TNF-α主要存在于鼻黏膜的柱状上皮、血管内皮、腺体及部分炎性细胞胞质中。AR大鼠鼻黏膜中TNF-α在蛋白和mRNA水平的表达均显著高于正常组（<0.01）。不同剂量18β-SGA干预后，TNF-α的表达均显著降低（<0.01），尤其是18β-SGA低剂量组干预4周后（<0.01）。不同剂量的18β-SGA对AR均有治疗作用，其作用机制可能与抑制TNF-α表达有关。
