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

  • Jae-Won Lee (Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Hyung Won Ryu (Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Su Ui Lee (Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Min-Gu Kim (Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Ok-Kyoung Kwon (Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Mun Ok Kim (Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Tae Kyu Oh (BTC Corporation, Technology Development Center) ;
  • Jae Kyoung Lee (BTC Corporation, Technology Development Center) ;
  • Tae Young Kim (BTC Corporation, Technology Development Center) ;
  • Sang Woo Lee (International Biological Material Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Sangho Choi (International Biological Material Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Wan-Yi Li (Institute of Medicinal Plants, Yunnan Academy of Agricultural Sciences) ;
  • Kyung-Seop Ahn (Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)) ;
  • Sei-Ryang Oh (Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB))
  • Published : 20190900

Abstract

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 α (TNF-α)-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 lipopolysaccharide (LPS). Treatment with PWRE significantly reduced the quantity of neutrophils and the levels of inflammatory molecules and toxic molecules, including tumor TNF-α, 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-κB 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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Acknowledgement

This research was supported by the Ministry of Trade, Industry and Energy (MOTIE) and the Korea Institute for the Advancement of Technology (KIAT) (grant no. N0002410, 2017).