Astaxanthin inhibits apoptosis in alveolar epithelial cells type II in vivo and in vitro through the ROS‐dependent mitochondrial signalling pathway

Journal of Cellular and Molecular Medicine

Xiaodong Song²  Bingsi Wang³  Shengcui Lin⁴  Lili Jing⁵  Cuiping Mao³  Pan Xu¹  Changjun Lv¹  Wen Liu² 

[1] Department of Respiratory Medicine, Affiliated Hospital to Binzhou Medical University, Binzhou, China;Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, China;Medicine Research Center, Binzhou Medical University, Yantai, China;Department of Respiratory Medicine, Affiliated Hospital to Binzhou Medical University, Yantai, China;Department of Pathology, Affiliated Hospital to Binzhou Medical University, Yantai, China

关键词: lung fibrosis;    oxidative stress;    astaxanthin;    ROS;    mitochondrial signalling pathway;   

DOI  :  10.1111/jcmm.12347

来源: Wiley

【 摘 要 】

Abstract

Oxidative stress is an important molecular mechanism underlying lung fibrosis. The mitochondrion is a major organelle for oxidative stress in cells. Therefore, blocking the mitochondrial signalling pathway may be the best therapeutic manoeuver to ameliorate lung fibrosis. Astaxanthin (AST) is an excellent antioxidant, but no study has addressed the pathway of AST against pulmonary oxidative stress and free radicals by the mitochondrion-mediated signalling pathway. In this study, we investigated the antioxidative effects of AST against H₂O₂- or bleomycin (BLM)-induced mitochondrial dysfunction and reactive oxygen species (ROS) production in alveolar epithelial cells type II (AECs-II) in vivo and in vitro. Our data show that AST blocks H₂O₂- or BLM-induced ROS generation and dose-dependent apoptosis in AECs-II, as characterized by changes in cell and mitochondria morphology, translocation of apoptotic proteins, inhibition of cytochrome c (Cyt c) release, and the activation of caspase-9, caspase-3, Nrf-2 and other cytoprotective genes. These data suggest that AST inhibits apoptosis in AECs-II cells through the ROS-dependent mitochondrial signalling pathway and may be of potential therapeutic value in lung fibrosis treatment.

【 授权许可】

CC BY   
© 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

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