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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Ursolic acid, a potential PPARγ agonist, suppresses ovalbumin-induced airway inflammation and Penh by down-regulating IL-5, IL-13, and IL-17 in a mouse model of allergic asthma
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Ursolic acid, a potential PPARγ agonist, suppresses ovalbumin-induced airway inflammation and Penh by down-regulating IL-5, IL-13, and IL-17 in a mouse model of allergic asthma

机译：潜在的PPARγ激动剂熊草酸通过下调过敏性哮喘小鼠模型中的IL-5，IL-13和IL-17抑制卵白蛋白诱导的气道炎症和Penh

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Allergic asthma is a chronic airway disorder characterized by airway hyperresponsiveness to allergens, chronic airway inflammation, airway edema, increased mucus secretion, excess production of Th2 cytokines, and eosinophil accumulation in the lungs. Ursolic acid is known for its pharmacological effects, such as its anti-tumor, anti-inflammatory and antimicrobial activities. To investigate the anti-asthmatic effects and mechanism of ursolic acid, we studied the development of pulmonary eosinophilic inflammation and enhanced pause (Penh) in a mouse model of allergic asthma. In this study, BALB/c mice were systemically sensitized to ovalbumin followed by intratracheal, intraperitoneal, and aerosol allergen challenges. We investigated the effect of ursolic acid and Cyclosporin A (CsA) on Penh, pulmonary eosinophilic infiltration, various immune cell phenotypes, Th2 cytokines, IL-17 production, and ovalbumin specific IgE production in a mouse model of asthma. In BALB/c mice, ursolic acid had suppressed eosinophil infiltration, allergic airway inflammation, and Penh, which occurred by suppressing the production of IL-5, IL-13, IL-17, and ovalbumin-specific IgE by blocking the GATA-3 and STAT6 pathways. Our data suggest the therapeutic mechanism of ursolic acid in asthma is based on reductions of Th2 cytokines (IL-5 and IL-13), ovalbumin-specific IgE production, and eosinophil infiltration via the Th2-GATA-3, STAT6, and IL-17-NF-κB pathways.
机译：过敏性哮喘是一种慢性气道疾病，其特征在于气道对过敏原反应过度，慢性气道炎症，气道水肿，粘液分泌增加，Th2细胞因子的过量产生以及肺中嗜酸性粒细胞的积累。熊果酸以其药理作用如抗肿瘤，抗炎和抗微生物活性而闻名。为了研究熊果酸的抗哮喘作用和机理，我们研究了过敏性哮喘小鼠模型中肺嗜酸性粒细胞炎症的发展和增强的停顿（Penh）。在这项研究中，BALB / c小鼠全身对卵清蛋白致敏，然后进行气管内，腹膜内和气溶胶过敏原攻击。我们研究了熊果酸和环孢菌素A（CsA）对哮喘小鼠模型中Penh，肺嗜酸性粒细胞浸润，各种免疫细胞表型，Th2细胞因子，IL-17产生和卵清蛋白特异性IgE产生的影响。在BALB / c小鼠中，熊果酸抑制嗜酸性粒细胞浸润，过敏性气道炎症和Penh，这是通过阻断GATA-3抑制IL-5，IL-13，IL-17和卵清蛋白特异性IgE的产生而发生的。和STAT6途径。我们的数据表明熊果酸在哮喘中的治疗机制是基于Th2细胞因子（IL-5和IL-13）减少，卵清蛋白特异性IgE产生以及嗜酸性粒细胞通过Th2-GATA-3，STAT6和IL- 17-NF-κB途径。

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