Asthma is recognized as a chronic respiratory illness characterized by airway inflammation and airway hyperresponsiveness. Wogonoside, a flavonoid glycoside, is reported to significantly alleviate the inflammation response and oxidative stress. Herein, this study aimed to investigate the therapeutic effect and underlying mechanism of wogonoside on airway inflammation and mucus hypersecretion in a murine asthma model and in human bronchial epithelial cells (16HBE). BALB/c mice were sensitized and challenged with ovalbumin (OVA). Pulmonary function and the number of cells in the bronchoalveolar lavage fluid (BALF) were examined. Pathological changes in lung tissue in each group were evaluated via hematoxylin and eosin and periodic acid–Schiff staining, and changes in levels of cytokines in BALF and of immunoglobulin E in serum were determined via an enzyme-linked immunosorbent assay. The expression of relevant genes in lung tissue was analyzed via real-time PCR. Western blotting and immunofluorescence were employed to detect the expression of relevant proteins in lung tissue and 16HBE cells. Treatment with 10 and 20 mg/kg wogonoside significantly attenuated the OVA-induced increase of inflammatory cell infiltration, mucus secretion, and goblet cell percentage and improved pulmonary function. Wogonoside treatment reduced the level of T-helper 2 cytokines including interleukin (IL)-4, IL-5, and IL-13 in BALF and of IgE in serum and decreased the mRNA levels of cytokines (IL-4, IL-5, IL-6, IL-13, and IL-1β and tumor necrosis factor-α), chemokines (CCL-2, CCL-11, and CCL-24), and mucoproteins (MUC5AC, MUC5B, and GOB5) in lung tissues. The expression of MUC5AC and the phosphorylation of STAT6 and NF-κB p65 in lung tissues and 16HBE cells were significantly downregulated after wogonoside treatment. Thus, wogonoside treatment may effectively decrease airway inflammation, airway remodeling, and mucus hypersecretion via blocking NF-κB/STAT6 activation.

中文翻译：

---

汉黄芩苷通过 NF-κB/STAT6 信号传导改善卵清蛋白诱导的小鼠急性哮喘中的气道炎症和粘液分泌过多

哮喘被认为是一种慢性呼吸道疾病，其特征是气道炎症和气道高反应性。据报道，汉黄芩苷是一种黄酮苷，可显着减轻炎症反应和氧化应激。本研究旨在探讨汉黄芩苷对小鼠哮喘模型和人支气管上皮细胞（16HBE）气道炎症和粘液分泌过多的治疗效果和潜在机制。 BALB/c 小鼠用卵清蛋白 (OVA) 致敏和攻击。检查肺功能和支气管肺泡灌洗液（BALF）中的细胞数量。采用苏木精、伊红和高碘酸希夫染色评价各组肺组织病理变化，并采用酶联免疫吸附法测定BALF中细胞因子和血清中免疫球蛋白E水平的变化。通过实时PCR分析肺组织中相关基因的表达。采用Western blotting和免疫荧光法检测肺组织和16HBE细胞中相关蛋白的表达。用 10 和 20 mg/kg 汉黄芩苷治疗可显着减弱 OVA 诱导的炎症细胞浸润、粘液分泌和杯状细胞百分比的增加，并改善肺功能。汉黄芩苷治疗降低了 BALF 中 T 辅助细胞 2 细胞因子的水平，包括白介素 (IL)-4、IL-5 和 IL-13 以及血清中 IgE 的水平，并降低了细胞因子（IL-4、IL-5、肺组织中的 IL-6、IL-13 和 IL-1β 以及肿瘤坏死因子-α)、趋化因子（CCL-2、CCL-11 和 CCL-24）和粘蛋白（MUC5AC、MUC5B 和 GOB5）。汉黄芩苷处理后肺组织和16HBE细胞中MUC5AC的表达以及STAT6和NF-κB p65的磷酸化显着下调。因此，汉黄芩苷治疗可以通过阻断 NF-κB/STAT6 激活来有效减少气道炎症、气道重塑和粘液分泌过多。