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葛根汤通过 IκBα/NF-κB 信号通路减轻香烟烟雾和脂多糖诱导的肺部炎症。

Galgeun-tang Attenuates Cigarette Smoke and Lipopolysaccharide Induced Pulmonary Inflammation via IκBα/NF-κB Signaling.

机构信息

College of Veterinary Medicine (BK21 Plus Project Team), Chonnam National University, 77 Yongbong-ro, Buk-gu, Gwangju 61186, Korea.

Herbal Medicinal Research Center, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, Korea.

出版信息

Molecules. 2018 Sep 28;23(10):2489. doi: 10.3390/molecules23102489.

DOI:10.3390/molecules23102489
PMID:30274192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6222390/
Abstract

Galgeun-tang water extract (GGWE) is used to treat various diseases such as the common cold, eczema and asthma in China and Korea. In this study, we investigated the anti-inflammatory effect of GGWE using a cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced induced pulmonary inflammation mouse model. The mice were exposed to CS for a total of seven days (eight cigarettes per day for 1 h) and LPS was administered intranasally to mice on day 4. GGWE was administered by oral gavage at doses of 50 mg/kg or 100 mg/kg 1 h before exposure to CS. GGWE decreased inflammatory cell counts, and expression of inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α) in bronchoalveolar lavage fluid (BALF) from mice exposed to CS and LPS. GGWE reduced the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the phosphorylation of inhibitor of kappa-B subunit alpha (IκBα) and nuclear factor kappa-B (NF-κB) in CS- and LPS-exposed mice. Histological examinations revealed that GGWE suppressed inflammatory cell infiltration into lung tissue compared to untreated CS- and LPS-exposed mice. In conclusion, GGWE effectively suppressed CS- and LPS-induced pulmonary inflammation. Our results indicate that GGWE may be used as a protective drug to control pulmonary inflammation diseases such as chronic obstructive pulmonary disease.

摘要

葛根汤水提取物(GGWE)在中国和韩国被用于治疗感冒、湿疹和哮喘等多种疾病。在这项研究中,我们使用香烟烟雾(CS)和脂多糖(LPS)诱导的肺部炎症小鼠模型来研究 GGWE 的抗炎作用。小鼠总共暴露于 CS 中 7 天(每天 8 支香烟,每次 1 小时),并在第 4 天对 LPS 进行鼻腔内给药。在暴露于 CS 之前 1 小时,以 50mg/kg 或 100mg/kg 的剂量通过口服灌胃给予 GGWE。GGWE 降低了 CS 和 LPS 暴露的小鼠支气管肺泡灌洗液(BALF)中的炎性细胞计数,以及白细胞介素(IL)-6 和肿瘤坏死因子-α(TNF-α)等炎性细胞因子的表达。GGWE 降低了诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的表达,以及 CS 和 LPS 暴露小鼠中κB 亚单位抑制蛋白-α(IκBα)和核因子 kappa-B(NF-κB)的磷酸化。组织学检查显示,与未治疗的 CS 和 LPS 暴露的小鼠相比,GGWE 抑制了炎性细胞浸润到肺组织中。总之,GGWE 有效抑制了 CS 和 LPS 诱导的肺部炎症。我们的结果表明,GGWE 可作为控制慢性阻塞性肺疾病等肺部炎症性疾病的保护药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/402d56820a25/molecules-23-02489-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/f28f87587725/molecules-23-02489-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/e840abf5f154/molecules-23-02489-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/234ff836fa9b/molecules-23-02489-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/cf47dc0832a8/molecules-23-02489-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/b7a6dfca8644/molecules-23-02489-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/402d56820a25/molecules-23-02489-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/f28f87587725/molecules-23-02489-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/e840abf5f154/molecules-23-02489-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/234ff836fa9b/molecules-23-02489-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/cf47dc0832a8/molecules-23-02489-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/b7a6dfca8644/molecules-23-02489-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1a/6222390/402d56820a25/molecules-23-02489-g007.jpg

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