Yukgunja-tang, a Traditional Herbal Formula, Attenuates Cigarette Smoke-induced Lung Inflammation in a Mouse Model

被引:1
作者
Park, Eunsook [1 ]
Jeon, Woo-Young [1 ]
Seo, Chang-Seob [1 ]
Ha, Hyekyung [1 ]
Jin, Seong Eun [1 ]
Kim, Jinhee [2 ]
Lee, Mee-Young [1 ]
机构
[1] Korea Inst Oriental Med, K Herb Res Ctr, 1672 Yuseong Daero, Daejeon 34054, South Korea
[2] Korea Inst Oriental Med, Herbal Med Res Div, 1672 Yuseong Gu, Daejeon 34054, South Korea
关键词
Chronic obstructive pulmonary disease; cigarette smoke; inflammatory cells; lung inflammation; Yukgunja-tang; OBSTRUCTIVE PULMONARY-DISEASE; NF-KAPPA-B; ACTIVATED PROTEIN-KINASE; AIRWAY INFLAMMATION; GASTROINTESTINAL SYMPTOMS; COPD; RIKKUNSHITO; PATHWAYS; ASTHMA; ROFLUMILAST;
D O I
10.4103/pm.pm_351_17
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Background: Chronic obstructive pulmonary disease is a progressive lung disease that involves airway inflammation, chronic bronchitis, and emphysema. Yukgunja-tang, one of the traditional Asian herbal medicines, has been used widely in treating patients with gastrointestinal diseases in Korea. Objective: Here, we investigated its efficacy on the inflammatory response using a mouse model of cigarette smoke (CS) exposure together with lipopolysaccharide (LPS) treatment. Materials and Methods: Over 4 weeks, mice were exposed to CS on 5 days/week and instilled intranasally with LPS on days 8 and 23. Yukgunja-tang water extract (YTWE) was administered to mice on the same 5 days. Results: YTWE administration significantly reduced the numbers of inflammatory cells and levels of pro-inflammatory cytokines in bronchoalveolar lavage fluid compared with CS plus LPS-exposed mice. Moreover, YTWE inhibited the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and I kappa B alpha proteins induced by CS plus LPS treatment. Histologically, YTWE attenuated the infiltration of inflammatory cells into peribronchial lesions, thickening of alveolar walls and accumulation of collagen in the lung tissues. Conclusion: Our findings suggest that YTWE prevents CS plus LPS-induced lung inflammation by inhibiting p38 MAPK and I.Ba signaling. Therefore, YTWE might be a potential drug for the treatment of lung inflammation induced by CS exposure.
引用
收藏
页码:275 / 282
页数:8
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