目的 觀察魚腥草素鈉對急性哮喘模型小鼠的抗炎作用，并探討作用機制。方法 建立卵白蛋白（OVA）誘導小鼠急性哮喘模型，將造模小鼠隨機分為模型組，魚腥草素鈉低、高劑量（10、25 mg/kg）組，每組8只，另取正常小鼠8只作為對照組，ig給藥2周，對照組與模型組給予等體積生理鹽水。采用小鼠肺功能儀器檢測小鼠氣道高反應(yīng)性；ELISA法檢測血清中特異性O(shè)VA-IgE、白細胞介素-4（IL-4）、單核細胞趨化因子-1（MCP-1）濃度；實時熒光定量PCR（qRT-PCR）法檢測肺組織中Toll樣受體-4（TLR-4）、髓樣分化因子88（MyD88）、轉(zhuǎn)鐵蛋白6（TRF6）mRNA的表達水平；HE染色后，光鏡觀察肺組織病理變化。結(jié)果 與模型組比較，10、25 mg/kg魚腥草素鈉組小鼠在乙酰甲膽堿激發(fā)濃度氣道高反應(yīng)值、血清OVE-IgE水平、血清IL-4和MCP濃度均顯著降低，具有統(tǒng)計學差異（P<0.05、0.01）；與模型組比較，10 mg/kg魚腥草素鈉組肺組織MyD88、TRF6 mRNA表達和25 mg/kg魚腥草素鈉組肺組織TLR-4、MyD88、TRF6 mRNA表達顯著降低，具有統(tǒng)計學差異（P<0.05、0.01）。HE染色顯示，魚腥草素鈉顯著改善模型小鼠的肺組織結(jié)構(gòu)紊亂、肺泡塌陷、支氣管周圍大量炎癥細胞浸潤、管腔內(nèi)有大量分泌物等癥狀。結(jié)論 魚腥草素鈉能顯著抑制急性哮喘模型小鼠的炎癥，機制可能與調(diào)節(jié)TLR4-NF-κB信號通路有關(guān)。

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.

R285.5

廣東省級科技計劃項目（2017A020215129）；廣東省中醫(yī)藥管理局項目（20181235）；湖南省衛(wèi)生計生委科研基金（132015-128）；深圳市科技計劃項目基礎(chǔ)研究（JCYJ20160429183052202）；深圳市南山區(qū)科技項目（2017016）