Shin Na-Rae, Park Sung-Hyeuk, Ko Je-Won, Ryu Hyung-Won, Jeong Seong-Hun, Kim Jong-Choon, Shin Dong-Ho, Lee Hoon-Sang, Shin In-Sik
College of Veterinary Medicine (BK21 project team), Chonnam National University, Gwangju, Korea.
Natural Medicine Research Center, Korea Research Institute of Bioscience & Biotechnology, Chungju, Korea.
Lab Anim Res. 2017 Sep;33(3):209-215. doi: 10.5625/lar.2017.33.3.209. Epub 2017 Sep 27.
is used as a health supplement, tea, and food source in Korea. This study aimed to evaluate the effect of (AA) and its active compound, dehydromatricarin A (DA), on the attenuation of airway inflammation in a murine model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). The C57BL/6 mice were administered AA (50 mg/kg or 100 mg/kg) and DA (10 mg/kg or 20 mg/kg) by oral gavage from day 0 to 7 days and LPS treated by intranasal instillation 48 hours before the sacrifice. The treatment of AA and DA markedly decreased inflammatory cells in the bronchoalveolar lavage fluid (BALF) compared with that in ALI-induced mice, which was accompanied by a significant reduction in the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in BALF. Furthermore, the administration of AA and DA clearly decreased inducible nitric oxide synthase (iNOS) expression and nuclear factor kappa B (NF-κB) phosphorylation in comparison with that in the ALI-induced mice. The histological examination of the lung tissue revealed that the administration of AA and DA suppressed the inflammatory cell infiltration into the peribronchial and alveolar lesions induced by LPS instillation. Collectively, our results indicated that AA and DA effectively decreased the airway inflammatory response induced by LPS instillation. Therefore, AA and DA may offer a potential therapy for airway inflammatory disease.
在韩国,它被用作健康补充剂、茶和食物来源。本研究旨在评估[物质名称未给出](AA)及其活性化合物脱氢马钱苷A(DA)对脂多糖(LPS)诱导的小鼠急性肺损伤(ALI)模型中气道炎症减轻的影响。从第0天到第7天,通过口服灌胃给予C57BL/6小鼠AA(50毫克/千克或100毫克/千克)和DA(10毫克/千克或20毫克/千克),并在处死前48小时通过鼻内滴注给予LPS。与ALI诱导的小鼠相比,AA和DA治疗显著减少了支气管肺泡灌洗液(BALF)中的炎症细胞,同时BALF中肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6水平显著降低。此外,与ALI诱导的小鼠相比,AA和DA的给药明显降低了诱导型一氧化氮合酶(iNOS)的表达和核因子κB(NF-κB)的磷酸化。肺组织的组织学检查显示,AA和DA的给药抑制了LPS滴注诱导的支气管周围和肺泡病变中的炎症细胞浸润。总体而言,我们的结果表明,AA和DA有效降低了LPS滴注诱导的气道炎症反应。因此,AA和DA可能为气道炎症性疾病提供一种潜在的治疗方法。