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首页> 外文期刊>International immunopharmacology >Antioxidant and antiasthmatic effects of saucerneol D in a mouse model of airway inflammation.
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Antioxidant and antiasthmatic effects of saucerneol D in a mouse model of airway inflammation.

机译:茶多酚D在气道炎症小鼠模型中的抗氧化和抗哮喘作用。

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摘要

Chronic airway inflammation is a hallmark of asthma, which is an immune-based disease. We evaluated the ability of saucerneol D, a tetrahydrofuran-type sesquilignan isolated from Saururus chinensis, to regulate airway inflammation in an ovalbumin (OVA)-induced airway inflammation model. Furthermore, we determined whether heme oxygenase (HO)-1 was required for the protective activity of saucerneol D. The airways of OVA-sensitized mice exposed to an OVA challenge developed eosinophilia and mucus hypersecretion and exhibited increased cytokine levels. Mice were administered saucerneol D orally at doses of 20 and 40mg/kg once daily on days 26-30. Saucerneol D administered orally significantly inhibited the number of OVA-induced inflammatory cells and the production of immunoglobulin E as well as Th2-type cytokines. Histopathology studies revealed a marked decrease in lung inflammation and goblet cell hyperplasia after saucerneol D treatment. In addition, saucerneol D induced HO-1 and led to a marked decrease in OVA-induced reactive oxygen species and malondialdehyde and an increase in superoxide dismutase and glutathione in lung tissues. These antioxidant effects were correlated with HO-1 induction. In our experiments, saucerneol D treatment reduced airway inflammation and suppressed oxidative stress in an OVA-induced asthma model.
机译:慢性气道炎症是哮喘的标志,哮喘是一种基于免疫的疾病。我们评估了从Saururus chinensis分离出的四氢呋喃型倍半萜烯sauceneol D在卵清蛋白(OVA)诱导的气道炎症模型中调节气道炎症的能力。此外,我们确定是否需要血红素加氧酶(HO)-1来保护邻苯三酚D。暴露于OVA的OVA致敏小鼠的气道发展为嗜酸性粒细胞增多和粘液分泌过多,并显示细胞因子水平升高。在第26-30天每天一次以20和40mg / kg的剂量口服给予鼠二酚D。口服saucerneol D显着抑制了OVA诱导的炎症细胞的数量以及免疫球蛋白E和Th2型细胞因子的产生。组织病理学研究显示,在使用satheneol D治疗后,肺部炎症和杯状细胞增生明显减少。此外,香豆酚D诱导HO-1,并导致OVA诱导的活性氧和丙二醛显着减少,肺组织中超氧化物歧化酶和谷胱甘肽增加。这些抗氧化作用与HO-1诱导相关。在我们的实验中,在OVA诱发的哮喘模型中,茶油酚D治疗可减少气道炎症并抑制氧化应激。

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