2. Academic Validation
  3. Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium

Astaxanthin attenuated cigarette smoke extract-induced apoptosis via decreasing oxidative DNA damage in airway epithelium

  • Biomed Pharmacother. 2023 Sep 10;167:115471. doi: 10.1016/j.biopha.2023.115471.
Hongmei Tang 1,  Yun Zhang 2,  Qiao Wang 1,  Ziling Zeng 1,  Xiaoyun Wang 1,  Yuejiao Li 1,  Zhibin Wang 1,  Ning Ma 1,  Guofeng Xu 1,  Xiaolin Zhong 3,  Linlin Guo 4,  Xiefang Yuan 5,  Xing Wang 6
Affiliations

Affiliations

  • 1 Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
  • 2 Inflammation & 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, China.
  • 3 Department of Gastroenterology Organization: The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
  • 4 Department 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. Electronic address: llinguo@iu.edu.
  • 5 Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. Electronic address: yxf_swmu@aliyun.com.
  • 6 Inflammation & Allergic Diseases Research Unit, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China. Electronic address: wx_eliot_881014@163.com.
PMID: 37699317 DOI: 10.1016/j.biopha.2023.115471
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.

Keywords

Astaxanthin; COPD; Cigarette smoke; DNA damage, Apoptosis; Inflammation; Lung disease; ROS.

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