牛蒡子苷元通过SIRT1/NLRP3途径减轻哮喘小鼠气道炎症

目的探讨牛蒡子苷元对哮喘小鼠模型中对气道炎症的疗效以及其机制是否与SIRT1/NLRP3信号通路有关。方法选取40只♀清洁级BALB/c小鼠,分为control组,OVA模型组,ATG组(5、10和20 mg·kg^-1)。HE及PAS染色法观察肺组织病理改变;Diff-Quick染色法对小鼠BALF中细胞分类及计数;流式细胞术测定小鼠肺组织中细胞因子在CD4阳性细胞群中的阳性比例;Western blot测定肺组织SIRT1、NLRP3、caspase-1、IL-18和IL-1β蛋白表达;免疫荧光法检测小鼠肺组织中NLRP3荧光强度。结果牛蒡子苷元能抑制OVA诱导的炎症细胞的渗出及杯状细胞增生;牛蒡子苷元抑制小鼠肺泡灌洗液中总细胞数及NEU、EOS、LYM的生成,并升高肺组织中IFN-γ水平的同时降低IL-4的水平;Western blot结果显示,牛蒡子苷元增加SIRT1蛋白表达同时抑制NLRP3、caspase-1、IL-18和IL-1β蛋白表达;免疫荧光结果显示,牛蒡子苷元可以减弱肺组织NLRP3的荧光强度。结论牛蒡子苷元通过SIRT1/NLRP3途径减轻哮喘小鼠气道炎症。

Arctigenin attenuates airway inflammation in asthmatic mice via SIRT1/NLRP3 pathway

Aim To investigate the efficacy of arctigenin on airway inflammation in a mouse model of asthma and the mechanism related to the SIRT1/NLRP3 signaling pathway.Methods Forty female BALB/c mice of clean grade were selected and divided into control group,OVA model group and ATG group(5,10 and 20 mg·kg^-1).HE and PAS staining were used to observe the pathological changes of lung tissues;Diff-Quick staining was used to classify and count the cells in BALF of mice;flow cytometry was used to determine the positive proportion of cytokines in the CD4-positive cell population in lung tissues of mice;Western blot was used to determine SIRT1,NLRP3,caspase-1,IL-18 and IL-1βprotein expression in lung tissues;immunofluorescence was used to detect NLRP3 fluorescence intensity in lung tissues of mice.Results Arctigenin inhibited OVA-induced exudation of inflammatory cells and goblet cell proliferation;arctigenin inhibited the number of total cells and the production of NEU,EOS,and LYM in mouse bronchoalveolar lavage fluid,and increased the level of IFN-γin lung tissues while decreased the level of IL-4;Western blot showed that arctigenin increased SIRT1 protein expression while inhibited NLRP3,caspase-1,IL-18,and IL-1β protein expression;immunofluorescence results showed that arctigenin could attenuate the fluorescence intensity of NLRP3 in lung tissues. Conclusion Arctigenin attenuates airway inflammation in asthmatic mice through SIRT1/NLRP3 signaling pathway.