Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium
Chronic obstructive pulmonary disease (COPD) is a lung inflammatory disease that is associated with environmental allergic component exposure. Cigarette smoke is an environmental toxicant that induces lung malfunction leading to various pulmonary diseases. Astaxanthin (AST) is a carotenoid that show...
| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-11-01
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| Series: | Biomedicine & Pharmacotherapy |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0753332223012696 |
| _version_ | 1797660592193929216 |
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| author | Hongmei Tang Yun Zhang Qiao Wang Ziling Zeng Xiaoyun Wang Yuejiao Li Zhibin Wang Ning Ma Guofeng Xu Xiaolin Zhong Linlin Guo Xiefang Yuan Xing Wang |
| author_facet | Hongmei Tang Yun Zhang Qiao Wang Ziling Zeng Xiaoyun Wang Yuejiao Li Zhibin Wang Ning Ma Guofeng Xu Xiaolin Zhong Linlin Guo Xiefang Yuan Xing Wang |
| author_sort | Hongmei Tang |
| collection | DOAJ |
| description | Chronic obstructive pulmonary disease (COPD) is a lung inflammatory disease that is associated with environmental allergic component exposure. Cigarette smoke is an environmental toxicant that induces lung malfunction leading to various pulmonary diseases. Astaxanthin (AST) is a carotenoid that shows antioxidant and anti-inflammatory activities which might be a promising candidate for COPD therapy. In this study, we released that AST could attenuate cigarette smoke-induced DNA damage and apoptosis in vivo and in vitro. AST administration ameliorated cigarette smoke extract (CSE)-induced activation of Caspase-3 and apoptosis. Pretreated mice with AST significantly decrease CSE-induced DNA damage which shows lower nuclear γ-H2AX level. AST treatment also dramatically reduces the production of intracellular reactive oxygen species (ROS) by suppressing the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme 4 (NOX4) and dual oxidase 1 (DUOX1). Taken together, this study suggested that AST can decrease CSE-induced DNA damage and apoptosis by inhibiting NOX4/DUOX1 expression that promotes ROS generation. AST may be a potential protective agent against CSE-associated lung disease that is worth in-depth investigation. |
| first_indexed | 2024-03-11T18:32:08Z |
| format | Article |
| id | doaj.art-99427d62ef2d45f79fcb26dea099aa0f |
| institution | Directory Open Access Journal |
| issn | 0753-3322 |
| language | English |
| last_indexed | 2024-03-11T18:32:08Z |
| publishDate | 2023-11-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Biomedicine & Pharmacotherapy |
| spelling | doaj.art-99427d62ef2d45f79fcb26dea099aa0f2023-10-13T11:02:44ZengElsevierBiomedicine & Pharmacotherapy0753-33222023-11-01167115471Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epitheliumHongmei Tang0Yun Zhang1Qiao Wang2Ziling Zeng3Xiaoyun Wang4Yuejiao Li5Zhibin Wang6Ning Ma7Guofeng Xu8Xiaolin Zhong9Linlin Guo10Xiefang Yuan11Xing Wang12Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China; Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaInflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaDepartment of Gastroenterology Organization: The Affiliated Hospital of Southwest Medical University, Luzhou 646000, ChinaDepartment of Microbiology and Immunology, The Indiana University School of Medicine, Indianapolis, IN 46202, USA; Department of Obstetrics and Gynecology, The Ohio State University Wexner Medical Center, The Ohio State University, Columbus, OH, USA; Corresponding author at: Department of Microbiology and Immunology, The Indiana University School of Medicine, Indianapolis, IN 46202, USA.Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China; Corresponding authors at: Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China; Corresponding authors at: Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.Chronic obstructive pulmonary disease (COPD) is a lung inflammatory disease that is associated with environmental allergic component exposure. Cigarette smoke is an environmental toxicant that induces lung malfunction leading to various pulmonary diseases. Astaxanthin (AST) is a carotenoid that shows antioxidant and anti-inflammatory activities which might be a promising candidate for COPD therapy. In this study, we released that AST could attenuate cigarette smoke-induced DNA damage and apoptosis in vivo and in vitro. AST administration ameliorated cigarette smoke extract (CSE)-induced activation of Caspase-3 and apoptosis. Pretreated mice with AST significantly decrease CSE-induced DNA damage which shows lower nuclear γ-H2AX level. AST treatment also dramatically reduces the production of intracellular reactive oxygen species (ROS) by suppressing the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme 4 (NOX4) and dual oxidase 1 (DUOX1). Taken together, this study suggested that AST can decrease CSE-induced DNA damage and apoptosis by inhibiting NOX4/DUOX1 expression that promotes ROS generation. AST may be a potential protective agent against CSE-associated lung disease that is worth in-depth investigation.http://www.sciencedirect.com/science/article/pii/S0753332223012696COPDAstaxanthinCigarette smokeDNA damage, ApoptosisROSInflammation |
| spellingShingle | Hongmei Tang Yun Zhang Qiao Wang Ziling Zeng Xiaoyun Wang Yuejiao Li Zhibin Wang Ning Ma Guofeng Xu Xiaolin Zhong Linlin Guo Xiefang Yuan Xing Wang Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium Biomedicine & Pharmacotherapy COPD Astaxanthin Cigarette smoke DNA damage, Apoptosis ROS Inflammation |
| title | Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium |
| title_full | Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium |
| title_fullStr | Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium |
| title_full_unstemmed | Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium |
| title_short | Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium |
| title_sort | astaxanthin attenuated cigarette smoke extract induced apoptosis via decreasing oxidative dna damage in airway epithelium |
| topic | COPD Astaxanthin Cigarette smoke DNA damage, Apoptosis ROS Inflammation |
| url | http://www.sciencedirect.com/science/article/pii/S0753332223012696 |
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