4.7 Article

Loranthus tanakae Franch. & Say. Suppresses Inflammatory Response in Cigarette Smoke Condensate Exposed Bronchial Epithelial Cells and Mice

Journal

ANTIOXIDANTS
Volume 11, Issue 10, Pages -

Publisher

MDPI
DOI: 10.3390/antiox11101885

Keywords

Loranthus tanakae Franch. & Sav; cigarette smoke condensate; chronic obstructive pulmonary disease; NF-kappa B; Nrf2

Funding

  1. National Research Council of Science and Technology [CRC21021]
  2. National Research Foundation of Korea - Korea Government [NRF-2020R1A4A1019395]
  3. [KSN2021320]

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The study found that Loranthus tanakae 70% ethanol extract (LTE) effectively alleviates pulmonary inflammation caused by exposure to cigarette smoke condensate and lipopolysaccharide by modulating the activity of Nrf2 and NF-κB, potentially making it a treatment option for pulmonary inflammatory diseases such as chronic obstructive pulmonary disease (COPD).
Loranthus tanakae Franch. & Sav. found in China, Japan, and Korea is traditionally used for managing arthritis and respiratory diseases. In this study, we analyzed the components of L. tanakae 70% ethanol extract (LTE) and investigated the therapeutic effects of LTE on pulmonary inflammation using cells exposed to cigarette smoke condensate (CSC) and lipopolysaccharide (LPS) in vitro and in vivo in mice and performed a network analysis between components and genes based on a public database. We detected quercitrin, afzelin, rhamnetin 3-rhamnoside, and rhamnocitrin 3-rhamnoside in LTE, which induced a significant reduction in inflammatory mediators including interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha and inflammatory cells in CSC exposed H292 cells and in mice, accompanied by a reduction in inflammatory cell infiltration into lung tissue. In addition, LTE increased translocation into the nuclei of nuclear factor erythroid-2-related factor 2 (Nrf2). By contrast, the activation of nuclear factor (NF)-kappa B, induced by CSC exposure, decreased after LTE application. These results were consistent with the network pharmacological analysis. In conclusion, LTE effectively attenuated pulmonary inflammation caused by CSC+LPS exposure, which was closely involved in the enhancement of Nrf2 expression and suppression of NF-kappa B activation. Therefore, LTE may be a potential treatment option for pulmonary inflammatory diseases including chronic obstructive pulmonary disease (COPD).

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