1. Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium.
- Author
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Tang, Hongmei, Zhang, Yun, Wang, Qiao, Zeng, Ziling, Wang, Xiaoyun, Li, Yuejiao, Wang, Zhibin, Ma, Ning, Xu, Guofeng, Zhong, Xiaolin, Guo, Linlin, Yuan, Xiefang, and Wang, Xing
- Subjects
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ASTAXANTHIN , *SMOKING , *CIGARETTE smoke , *DNA damage , *CELL death , *NICOTINAMIDE adenine dinucleotide phosphate , *CHRONIC obstructive pulmonary disease - Abstract
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. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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