Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cells
Background: Methyl lucidone (ML), a methyl derivative of lucidone, has anti-inflammatory properties. However, the molecular mechanisms that reduce the inflammatory effect of ML in human lung epithelial cells remain unkown. This study aimed to elucidate the molecular mechanisms underlying the anti-in...
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| Format: | Article |
| Language: | English |
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Elsevier
2023-09-01
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| Series: | Heliyon |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844023073620 |
| _version_ | 1797669712085123072 |
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| author | Eun Sol Oh Hyunju Ro Hyung Won Ryu Yu Na Song Ji-Yoon Park Namho Kim Hae-Young Kim Seon Min Oh Su-Yeon Lee Doo-Young Kim Sooil Kim Sung-Tae Hong Mun-Ock Kim Su Ui Lee |
| author_facet | Eun Sol Oh Hyunju Ro Hyung Won Ryu Yu Na Song Ji-Yoon Park Namho Kim Hae-Young Kim Seon Min Oh Su-Yeon Lee Doo-Young Kim Sooil Kim Sung-Tae Hong Mun-Ock Kim Su Ui Lee |
| author_sort | Eun Sol Oh |
| collection | DOAJ |
| description | Background: Methyl lucidone (ML), a methyl derivative of lucidone, has anti-inflammatory properties. However, the molecular mechanisms that reduce the inflammatory effect of ML in human lung epithelial cells remain unkown. This study aimed to elucidate the molecular mechanisms underlying the anti-inflammatory effect of ML. Methods: Four compounds (ML, methyl linderone, kanakugiol, and linderone) from Lindera erythrocarpa Makino were evaluated for their ability to reduce MUC5AC secretion levels in phorbol-12-myristate-13-acetate (PMA)-stimulated NCI–H292 cells using ELISA. The expression and secretion levels of inflammatory response-related proteins were analyzed using quantitative reverse transcription-PCR, ELISA, and western blotting. To determine whether ML directly regulates TGF-β-activated kinase 1 (TAK1), we performed an in vitro kinase assay. Results: ML treatment effectively reduced the levels of inflammatory cytokines, including interleukin-1β and TNF-α, increased by stimulation. Furthermore, ML downregulated the pathway cascade of both IκB kinase (IKK)/NF-κB and p38 mitogen-activated protein (MAP) kinase/CREB by inhibiting the upstream kinase TAK1. An in vitro kinase analysis confirmed that ML treatment significantly reduced the kinase activity of TAK1. Conclusion: ML pretreatment repressed the PMA-stimulated inflammation reaction by reducing the TAK1-mediated IKK/NF-κB and p38 MAP kinase/CREB signaling. These findings suggest that ML may improve respiratory health and can be used as a dietary supplement or functional food to prevent inflammatory lung diseases. |
| first_indexed | 2024-03-11T20:48:29Z |
| format | Article |
| id | doaj.art-78c60934c724491e95f7411258bf8669 |
| institution | Directory Open Access Journal |
| issn | 2405-8440 |
| language | English |
| last_indexed | 2024-03-11T20:48:29Z |
| publishDate | 2023-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj.art-78c60934c724491e95f7411258bf86692023-10-01T06:02:43ZengElsevierHeliyon2405-84402023-09-0199e20154Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cellsEun Sol Oh0Hyunju Ro1Hyung Won Ryu2Yu Na Song3Ji-Yoon Park4Namho Kim5Hae-Young Kim6Seon Min Oh7Su-Yeon Lee8Doo-Young Kim9Sooil Kim10Sung-Tae Hong11Mun-Ock Kim12Su Ui Lee13Natural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea; Department of Biological Sciences, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, 34134, Republic of KoreaDepartment of Biological Sciences, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, 34134, Republic of KoreaNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of KoreaNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea; Department of Biological Sciences, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, 34134, Republic of KoreaNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea; Department of Anatomy and Cell Biology, Department of Medical Science, College of Medicine, Chungnam National University, Daejeon, 35015, Republic of KoreaNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea; Department of Anatomy and Cell Biology, Department of Medical Science, College of Medicine, Chungnam National University, Daejeon, 35015, Republic of KoreaNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of KoreaNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of KoreaNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of KoreaNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of KoreaDepartment of Anatomy and Cell Biology, Department of Medical Science, College of Medicine, Chungnam National University, Daejeon, 35015, Republic of KoreaDepartment of Anatomy and Cell Biology, Department of Medical Science, College of Medicine, Chungnam National University, Daejeon, 35015, Republic of Korea; Corresponding author.Natural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea; Corresponding author.Natural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungbuk, 28116, Republic of Korea; Corresponding author.Background: Methyl lucidone (ML), a methyl derivative of lucidone, has anti-inflammatory properties. However, the molecular mechanisms that reduce the inflammatory effect of ML in human lung epithelial cells remain unkown. This study aimed to elucidate the molecular mechanisms underlying the anti-inflammatory effect of ML. Methods: Four compounds (ML, methyl linderone, kanakugiol, and linderone) from Lindera erythrocarpa Makino were evaluated for their ability to reduce MUC5AC secretion levels in phorbol-12-myristate-13-acetate (PMA)-stimulated NCI–H292 cells using ELISA. The expression and secretion levels of inflammatory response-related proteins were analyzed using quantitative reverse transcription-PCR, ELISA, and western blotting. To determine whether ML directly regulates TGF-β-activated kinase 1 (TAK1), we performed an in vitro kinase assay. Results: ML treatment effectively reduced the levels of inflammatory cytokines, including interleukin-1β and TNF-α, increased by stimulation. Furthermore, ML downregulated the pathway cascade of both IκB kinase (IKK)/NF-κB and p38 mitogen-activated protein (MAP) kinase/CREB by inhibiting the upstream kinase TAK1. An in vitro kinase analysis confirmed that ML treatment significantly reduced the kinase activity of TAK1. Conclusion: ML pretreatment repressed the PMA-stimulated inflammation reaction by reducing the TAK1-mediated IKK/NF-κB and p38 MAP kinase/CREB signaling. These findings suggest that ML may improve respiratory health and can be used as a dietary supplement or functional food to prevent inflammatory lung diseases.http://www.sciencedirect.com/science/article/pii/S2405844023073620Methyl lucidoneInflammatory lung diseaseTAK1NF-κBp38 MAP kinaseHuman bronchial epithelial cell |
| spellingShingle | Eun Sol Oh Hyunju Ro Hyung Won Ryu Yu Na Song Ji-Yoon Park Namho Kim Hae-Young Kim Seon Min Oh Su-Yeon Lee Doo-Young Kim Sooil Kim Sung-Tae Hong Mun-Ock Kim Su Ui Lee Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cells Heliyon Methyl lucidone Inflammatory lung disease TAK1 NF-κB p38 MAP kinase Human bronchial epithelial cell |
| title | Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cells |
| title_full | Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cells |
| title_fullStr | Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cells |
| title_full_unstemmed | Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cells |
| title_short | Methyl lucidone inhibits airway inflammatory response by reducing TAK1 activity in human bronchial epithelial NCI–H292 cells |
| title_sort | methyl lucidone inhibits airway inflammatory response by reducing tak1 activity in human bronchial epithelial nci h292 cells |
| topic | Methyl lucidone Inflammatory lung disease TAK1 NF-κB p38 MAP kinase Human bronchial epithelial cell |
| url | http://www.sciencedirect.com/science/article/pii/S2405844023073620 |
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