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Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide-induced pulmonary inflammation by inhibiting interleukin-8 production and NF-kappa B activation

文献类型： 外文期刊

作者： Lee, Jae-Won 1 ; Ryu, Hyung Won 1 ; Lee, Su Ui 1 ; Kim, Min-Gu 1 ; Kwon, Ok-Kyoung 1 ; Kim, Mun Ok 1 ; Oh, Tae Kyu 2 ; Le 1 ;

作者机构： 1.KRIBB, Nat Med Res Ctr, 30 Yeongudanji Ro, Cheongju 28116, Chungcheongbuk, South Korea

2.BTC Corp, Technol Dev Ctr, Ansan 15588, Gyeonggi Do, South Korea

3.KRIBB, Int Biol Mat Res Ctr, Daejeon 34141, South Korea

4.Yunnan Acad Agr Sci, Inst Med Plants, Kunming 650200, Yunnan, Peoples R China

关键词： Pistacia weinmannifolia; chronic obstructive pulmonary disease; airway inflammation; neutrophils; NF-kappa B; interleukin-8

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE （ 影响因子：4.101； 五年影响因子：4.084 ）

ISSN： 1107-3756

年卷期： 2019 年 44 卷 3 期

页码：

收录情况： SCI

摘要： Pistacia weinmannifolia (PW) has been used in traditional Chinese medicine to treat headaches, dysentery, enteritis and influenza. However, PW has not been known for treating respiratory inflammatory diseases, including chronic obstructive pulmonary disease (COPD). The present in vitro analysis confirmed that PW root extract (PWRE) exerts anti-inflammatory effects in phorbol myristate acetate- or tumor necrosis factor alpha (TNF-alpha)-stimulated human lung epithelial NCI-H292 cells by attenuating the expression of interleukin (IL)-8, IL-6 and Mucin A5 (MUC5AC), which are closely associated with the pulmonary inflammatory response in the pathogenesis of COPD. Thus, the aim of the present study was to evaluate the protective effect of PWRE on pulmonary inflammation induced by cigarette smoke (CS) and lipopoly-saccharide (LPS). Treatment with PWRE significantly reduced the quantity of neutrophils and the levels of inflammatory molecules and toxic molecules, including tumor TNF-alpha, IL-6, IL-8, monocyte chemoattractant protein-1, neutrophil elastase and reactive oxygen species, in the bronchoalveolar lavage fluid of mice with CS- and LPS-induced pulmonary inflammation. PWRE also attenuated the influx of inflammatory cells in the lung tissues. Furthermore, PWRE downregulated the activation of nuclear factor-kappa B and the expression of phosphodiesterase 4 in the lung tissues. Therefore, these findings suggest that PWRE may be a valuable adjuvant treatment for COPD.

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