1. Academic Validation
  2. 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.
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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