目的 观察鱼腥草素钠对急性哮喘模型小鼠的抗炎作用，并探讨作用机制。方法 建立卵白蛋白（OVA）诱导小鼠急性哮喘模型，将造模小鼠随机分为模型组，鱼腥草素钠低、高剂量（10、25 mg/kg）组，每组8只，另取正常小鼠8只作为对照组，ig给药2周，对照组与模型组给予等体积生理盐水。采用小鼠肺功能仪器检测小鼠气道高反应性；ELISA法检测血清中特异性OVA-IgE、白细胞介素-4（IL-4）、单核细胞趋化因子-1（MCP-1）浓度；实时荧光定量PCR（qRT-PCR）法检测肺组织中Toll样受体-4（TLR-4）、髓样分化因子88（MyD88）、转铁蛋白6（TRF6）mRNA的表达水平；HE染色后，光镜观察肺组织病理变化。结果 与模型组比较，10、25 mg/kg鱼腥草素钠组小鼠在乙酰甲胆碱激发浓度气道高反应值、血清OVE-IgE水平、血清IL-4和MCP浓度均显著降低，具有统计学差异（P<0.05、0.01）；与模型组比较，10 mg/kg鱼腥草素钠组肺组织MyD88、TRF6 mRNA表达和25 mg/kg鱼腥草素钠组肺组织TLR-4、MyD88、TRF6 mRNA表达显著降低，具有统计学差异（P<0.05、0.01）。HE染色显示，鱼腥草素钠显著改善模型小鼠的肺组织结构紊乱、肺泡塌陷、支气管周围大量炎症细胞浸润、管腔内有大量分泌物等症状。结论 鱼腥草素钠能显著抑制急性哮喘模型小鼠的炎症，机制可能与调节TLR4-NF-κB信号通路有关。

Objective To observe the anti-inflammatory effects of sodium houttuyfonate (SH) on mice with acute asthma and to explore the specific mechanism. Methods OVA-induced acute asthma model in mice was established. The model mice were randomly divided into model group, low and high doses of sodium houttuynin (10, 25 mg/kg) group, 8 mice in each group, and 8 normal mice were taken as control group. After 2 weeks of Ig administration, the control group and model group were given normal saline of equal volume. The airway hyperresponsiveness of mice was measured by pulmonary function instrument, the specific concentrations of OVA-IgE, IL-4 and MCP-1 in serum were detected by ELISA, and the mRNA expression levels of Toll-like receptor-4 (TLR-4), myeloid differentiation factor 88 (MyD88) and transferrin 6 (TRF6) in lung tissue were detected by real-time fluorescence quantitative PCR (qRT-PCR). After HE staining, the pathological changes of lung tissue were observed under light microscope. Results Compared with the model group, the airway hyperresponsiveness, serum OVE-IgE level, serum IL-4 and MCP levels of mice in 10 and 25 mg/kg sodium houttuynin group were significantly decreased (P<0.05, 0.01); Compared with the model group, the expression of MyD88, TRF6 in lung tissue of 10 mg/kg sodium houttuynin group and TLR-4, MyD88, MyD88, and MCP in lung tissue of 25 mg/kg sodium houttuynin group were significantly decreased (P<0.05, 0.01). HE staining showed that sodium houttuynin significantly improved the symptoms of pulmonary tissue disorder, alveolar collapse, infiltration of inflammatory cells around the bronchi, and a large number of secretions in the lumen of the model mice. Conclusion Sodium houttuynia significantly inhibited inflammation in an acute asthma mice model and the mechanism may be related to the regulation of the TLR-4-NF-κB signaling pathway.

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广东省级科技计划项目（2017A020215129）；广东省中医药管理局项目（20181235）；湖南省卫生计生委科研基金（132015-128）；深圳市科技计划项目基础研究（JCYJ20160429183052202）；深圳市南山区科技项目（2017016）